 Cardio-ventilatory interaction recently has been studied through the heart rate variability in critically ill mechanical ventilated patients. The analysis of the power spectrum density provides information about the power the variance of beat-to-beat interval is distributed as frequencies function. Healthy spontaneously breathing subjects show a cyclic inspiratory increase and expiratory decrease of heart rate, and phase coupling between heart beats and respiration causing heart beats to occur at constant phases of the respiratory cycle, commonly known as cardioventilatory coupling. These phenomena originate from a complex interplay of several mechanisms including central drive, feedback from arterial baroreceptors, feedback from thoracic and lung stretch receptors, and non-neural mechanisms intrinsic to the heart, which are not fully understood. Although the physiological importance of respiratory sinus arrhythmia and cardioventilatory coupling have not been elucidated, several authors suggested that they might improve ventilationperfusion matching through a redistribution of heart beats and consequently of perfusion within the respiratory cycle, with beneficial effects on gas exchange. Furthermore, decreased respiratory sinus arrhythmia amplitude has been used as an indicator of impaired autonomic control and of poor clinical outcome, also during mechanical ventilation.It has been shown that during controlled mechanical ventilation the respiratory sinus arrhythmia amplitude is considerably reduced and the cardioventilatory coupling generally abolished. Theoretically, mechanical ventilation modes that assist the respiratory pump upon triggering by the patient, such as pressure support ventilation PSV might maintain higher respiratory sinus arrhythmia levels through centrally-originated phasic vagal modulation compared to controlled mechanical ventilation. In addition, mechanical ventilation with breath-by-breath variable tidal volumes, so-called variable ventilation, could better preserve respiratory sinus arrhythmia and cardioventilatory coupling, and this might play a role in the improved arterial oxygenation found in different models of acute lung injury, although with variable results, when comparing variable and conventional mechanical ventilation. In anesthetized experimental animals the cardioventilatory coupling was more preserved during pressure assisted ventilation than pressure controlled ventilation. If these findings could be present in the humans is yet unknown. Furthermore, it has been demonstrated that some new methodologies of assisted ventilation, such as the neurally adjusted ventilatory assist NAVA, increase the breath-to-breath variability and tidal volume variability, but their effects on cardioventilatory coupling are not understood. 