Effects of assisted and variable mechanical ventilation on cardiorespiratory interactions in anesthetized pigs

• Published in: Physiological measurement Vol. 33; no. 3; pp. 503 - 519
• Main Authors: Beda, Alessandro, Güldner, Andreas, Simpson, David M, Carvalho, Nadja C, Franke, Susanne, Uhlig, Christopher, Koch, Thea, Pelosi, Paolo, de Abreu, Marcelo Gama
• Format: Journal Article
• Language: English
• Published: England IOP Publishing 01.03.2012
• Subjects: Anesthesia; Animals; assisted mechanical ventilation; baroreflex; Cardiovascular Physiological Phenomena; cardioventilatory coupling; controlled mechanical ventilation; Female; Oxygen - blood; Respiration, Artificial - methods; Respiratory Physiological Phenomena; respiratory sinus arrhythmia; Swine; variable ventilation
• ISSN: 0967-3334; 1361-6579
• DOI: 10.1088/0967-3334/33/3/503

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 (VT), 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 VT, 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 VT 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.