Restoration of hemodynamics in apnea struggle phase in association with involuntary breathing movements

Abstract

Involuntary breathing movements (IBM) that occur in the struggle phase of maximal apneas produce waves of negative intrathoracic pressure. This could augment the venous return, increasing thereby the cardiac output and gas exchange, and release the fresh blood from venous pools of spleen and liver. To test these hypotheses we used photoplethysmography and ultrasound for assessment of hemodynamics and spleen size before, during and after maximal dry apneas at large lung volume in 7 trained divers. During the easy-going phase cardiac output was reduced about 40%, due to reduction in stroke volume and in presence of reduced inferior vena cava venous return, while the spleen contracted for about 60 ml. Towards the end of the struggle phase, in presence of intense IBM, the spleen volume further decreased for about 70 ml, while cardiac output and caval flow almost renormalized. In conclusion, IBM coincide with splenic volume reduction and restoration of hemodynamics, likely facilitating the use of the last oxygen reserves before apnea cessation.

Introduction

The diving response in humans is triggered by breath-hold and accentuated by face immersion. The responses include bradycardia (Asmussen and Kristiansson, 1968) and increased arterial blood pressure, caused by vasoconstriction of selected vascular beds (Leuenberger et al., 2001, Elsner et al., 1971), due to increased sympathetic efferent nerve activity towards skeletal muscle (Leuenberger et al., 2001). The purpose seems to be the redistribution of cardiac output to heart and brain, in conjunction with reduced overall oxygen consumption and work of heart, which could increase the breath-hold time.

Maximal voluntary apnea is divided into the “easy-going phase”, which lasts until “physiological breaking point”, at which time increased partial pressures of carbon dioxide (CO₂) stimulate respiratory drive (Lin, 1982), and the “struggle phase”, during which the subject feels a growing urge to breathe and shows progressive involuntary breathing movements (IBM) (Dejours, 1965, Hentsch and Ulmer, 1984). The tolerance to high PCO₂ and low PO₂ during voluntary apnea is much less than during rebreathing from the bag, suggesting that the stimulus to resume breathing has two components, a chemical one (PCO₂) and a mechanical one, triggered by non-expansion of the lungs (Kobayasi and Sasaki, 1967, Godfrey and Campbell, 1968).

The mechanical component seems to become active in the struggle phase of apnea, in association with IBM. The arguments for this were provided by Godfrey and Campbell (1968), who reported that paralysis of respiratory muscles increases the tolerance to absence of ventilation in comparison to voluntary breath-holding. Whitelaw et al. (1981) further evaluated this issue by assessing the strength of IBM, given by the magnitude of the negative intrathoracic pressure they produce. Unexpectedly, they did not find the correlation between the magnitude of IBM and the degree of dyspnea. To us these findings have a plausible background. Since IBM produce rather large increases in negativity of intrathoracic pressure, a consequent rise in venous return and cardiac output, in conjunction with mobilization of fresh blood from the spleen and liver are their expected effects. Thus, we put forward the hypothesis that IBM are associated with both, dyspnea signals and beneficial hemodynamic changes that facilitate the use of the remaining gas exchange reserves, attenuating the chemical drive to resumption of breathing. To investigate this hypothesis we tracked the cardiac output (CO), inferior vena cava (IVC) venous return, and splenic volumes during maximal apneas in trained apnea divers to see whether IBM, detected by respiratory belt, are associated with changes in these variables.