Frazier S K, Moser D K, Stone K S
Department of Adult Health & Illness, Ohio State University, USA.
Biol Res Nurs. 2001 Jan;2(3):167-74. doi: 10.1177/109980040100200302.
Variations in intrathoracic pressure generated by different ventilator weaning modes may significantly affect intrathoracic hemodynamics and cardiovascular stability. Although several investigators have attributed cardiovascular alterations during ventilator weaning to augmented sympathetic tone, there is limited investigation of changes in autonomic tone during ventilator weaning. Heart rate variability (HRV), the analysis of beat-to-beat changes in heart rate, is a noninvasive indicator of autonomic tone that might be useful in the identification of patients who are at risk for weaning difficulty due to underlying cardiac dysfunction. The authors describe HRV and hemodynamics in response to 3 ventilatory conditions: pressure support (PS) 10 cmH2O, continuous positive airway pressure (CPAP) 10 cmH2O, and a combination of PS 10 cmH2O and CPAP 10 cmH2O (PS + CPAP) in a group of canines with normal ventricular function. Six canines were studied in the laboratory. Continuous 3-lead electrocardiographic data were collected during baseline (controlled mechanical ventilation) and following transition to each of the ventilatory conditions (PS, CPAP, PS + CPAP) for analysis of HRV. HRV was evaluated using power spectral analysis to define the power under the curve in a very low frequency range (0.0033 to < 0.04 Hz, sympathetic tone), a low frequency range (0.04 to < 0.15 Hz, primarily sympathetic tone), and a high frequency range (0.15 to < 0.40 Hz, parasympathetic tone). A thermodilution pulmonary artery catheter measured cardiac output and right ventricular end-diastolic volume to describe global hemodynamics. There were significant increases in very low frequency power (sympathetic tone) with a concomitant significant reduction in high-frequency power (parasympathetic tone) with exposure to PS + CPAP. These alterations in HRV were associated with significantly increased heart rate and reduced right ventricular end-diastolic volume. Although there was a small but significant increase in cardiac output with exposure to PS, HRV was unchanged. These data indicate that there was a relative shift in autonomic balance to increased sympathetic and decreased parasympathetic tone with exposure to PS + CPAP. The increase in intrathoracic pressure reduced right ventricular end-diastolic volume (preload). This hemodynamic alteration generated a change in autonomic tone, so that cardiac output could be maintained. Individuals with autonomic and/or cardiovascular dysfunction may not be capable of this type of response and may fail to successfully wean from mechanical ventilation.
不同撤机模式产生的胸内压变化可能会显著影响胸内血流动力学和心血管稳定性。尽管有几位研究者将撤机过程中的心血管改变归因于交感神经张力增强,但对于撤机过程中自主神经张力变化的研究却很有限。心率变异性(HRV),即对逐搏心率变化的分析,是自主神经张力的一种非侵入性指标,可能有助于识别因潜在心脏功能障碍而有撤机困难风险的患者。作者描述了一组心室功能正常的犬在三种通气条件下的HRV和血流动力学情况:压力支持(PS)10 cmH₂O、持续气道正压通气(CPAP)10 cmH₂O以及PS 10 cmH₂O与CPAP 10 cmH₂O联合使用(PS + CPAP)。在实验室对6只犬进行了研究。在基线期(控制机械通气)以及转换至每种通气条件(PS、CPAP、PS + CPAP)后,收集连续三导联心电图数据以分析HRV。使用功率谱分析评估HRV,以确定极低频范围(0.0033至<0.04 Hz,交感神经张力)、低频范围(0.04至<0.15 Hz,主要为交感神经张力)和高频范围(0.15至<0.40 Hz,副交感神经张力)曲线下的功率。通过热稀释肺动脉导管测量心输出量和右心室舒张末期容积以描述整体血流动力学情况。暴露于PS + CPAP时,极低频功率(交感神经张力)显著增加,同时高频功率(副交感神经张力)显著降低。这些HRV的改变与心率显著增加和右心室舒张末期容积减少有关。尽管暴露于PS时心输出量有小幅但显著的增加,但HRV未发生变化。这些数据表明,暴露于PS + CPAP时,自主神经平衡相对向交感神经增强和副交感神经减弱的方向转变。胸内压升高降低了右心室舒张末期容积(前负荷)。这种血流动力学改变导致自主神经张力发生变化,从而维持心输出量。自主神经和/或心血管功能障碍的个体可能无法产生这种类型的反应,可能无法成功撤机。