Why the study?
What physiological mechanisms drive the decrease in left ventricular stroke volume during obstructive sleep-disordered breathing?
What physiological mechanisms drive the decrease in left ventricular stroke volume during obstructive sleep-disordered breathing?
Simulations suggest that decreased myocardial distensibility and fluid migration are primary drivers of the stroke volume decline in obstructive sleep-disordered breathing.
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Simulation findings on LVSV mechanisms in sleep-disordered breathing remain hypothesis-generating; prospective validation required before clinical application.
Background . Increased negative intrathoracic pressures are recognized to exacerbate left ventricular dysfunction in obstructive sleep-disordered breathing. Reportedly left ventricular stroke volume (LVSV) decline appeared greater than predicted by the obstruction alone. Objectives . Whether this effect is more dependent on biventricular elasticity and fluid shifts than on breathing-related transmural pressures could be inferred from a mathematical model simulation. Design . A previously validated cardiopulmonary model in healthy subjects during inspiratory loading was modified by parameter adjustments to fit its ventricular volumes output to published clinical data of decreased LVSV in obstructed breathing. Results . Reduced left ventricular end-diastolic compliance and increased central blood volume from baseline each simulated a 20% drop in LVSV whereas twice as much change was the result of increasing a mere 400 mL to the unstressed volume of systemic veins. An intermediate value was obtained by decreasing right ventricular end-diastolic compliance and higher systemic venous compliance. Conclusions . Simulations encompassing a wide range of decreased stroke volume at comparable intrathoracic pressures suggested a prominent role of decreased myocardial distensibility (possibly coupled to fluid migration) in the stroke volume fall.
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Ernesto Goldman (2012) studied this question.
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