Key result
Pressure assisted ventilation increased respiratory sinus arrhythmia amplitude to 50 ms compared to 20 ms with pressure controlled ventilation (p < 0.05) in anesthetized pigs.
Why the study?
Does pressure assisted ventilation compared to pressure controlled ventilation affect respiratory sinus arrhythmia and cardioventilatory coupling in anesthetized pigs?
Does pressure assisted ventilation compared to pressure controlled ventilation affect respiratory sinus arrhythmia and cardioventilatory coupling in anesthetized pigs?
Absolute Event Rate: 50% vs 20%
p-value: p=< 0.05
In anesthetized pigs, pressure assisted ventilation increases respiratory sinus arrhythmia amplitude and cardioventilatory coupling compared to pressure controlled ventilation, suggesting these changes reflect ventilation mode rather than autonomic impairment.
Supports further investigation of assisted ventilation on autonomic coupling; does not yet inform clinical strategies.
The physiological importance of respiratory sinus arrhythmia (RSA) and cardioventilatory coupling (CVC) has not yet been fully elucidated, but these phenomena might contribute to improve ventilation/perfusion matching, with beneficial effects on gas exchange. Furthermore, decreased RSA amplitude has been suggested as an indicator of impaired autonomic control and poor clinical outcome, also during positive-pressure mechanical ventilation (MV). However, it is currently unknown how different modes of MV, including variable tidal volumes (V(T)), affect RSA and CVC during anesthesia. We compared the effects of pressure controlled (PCV) versus pressure assisted (PSV) ventilation, and of random variable versus constant V(T), on RSA and CVC in eight anesthetized pigs. At comparable depth of anesthesia, global hemodynamics, and ventilation, RSA amplitude increased from 20 ms in PCV to 50 ms in PSV (p < 0.05). CVC was detected (using proportional Shannon entropy of the interval between each inspiration onset and the previous R-peak in ECG) in two animals in PCV and seven animals in PSV. Variable V(T) did not significantly influence these phenomena. Furthermore, heart period and systolic arterial pressure oscillations were in phase during PCV but in counter-phase during PSV. At the same depth of anesthesia in pigs, PSV increases RSA amplitude and CVC compared to PCV. Our data suggest that the central respiratory drive, but not the baroreflex or the mechano-electric feedback in the heart, is the main mechanism behind the RSA increase. Hence, differences in RSA and CVC between mechanically ventilated patients might reflect the difference in ventilation mode rather than autonomic impairment. Also, since gas exchange did not increase from PCV to PSV, it is questionable whether RSA has any significance in improving ventilation/perfusion matching during MV.
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Beda et al. (2012) studied Anesthetized pigs (n=8). Pressure assisted ventilation (PSV) vs. Pressure controlled ventilation (PCV) was evaluated on Respiratory sinus arrhythmia (RSA) amplitude (p=< 0.05). Pressure assisted ventilation increased respiratory sinus arrhythmia amplitude to 50 ms compared to 20 ms with pressure controlled ventilation (p < 0.05) in anesthetized pigs.
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