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容量控制通气和压力控制通气中的平台压与驱动压:小儿急性呼吸窘迫综合征中摩擦性和粘弹性阻力成分的比较

Plateau Pressure and Driving Pressure in Volume- and Pressure-Controlled Ventilation: Comparison of Frictional and Viscoelastic Resistive Components in Pediatric Acute Respiratory Distress Syndrome.

作者信息

Cruces Pablo, Moreno Diego, Reveco Sonia, Ramirez Yenny, Díaz Franco

机构信息

Departamento de Pediatría, Unidad de Paciente Crítico Pediátrico, Hospital El Carmen de Maipú, Santiago, Chile.

Centro de Investigación de Medicina Veterinaria, Escuela de Medicina Veterinaria, Facultad de Ciencias de la Vida, Universidad Andres Bello, Santiago, Chile.

出版信息

Pediatr Crit Care Med. 2023 Sep 1;24(9):750-759. doi: 10.1097/PCC.0000000000003291. Epub 2023 Jun 1.

DOI:10.1097/PCC.0000000000003291
PMID:37260322
Abstract

OBJECTIVES

To examine frictional, viscoelastic, and elastic resistive components, as well threshold pressures, during volume-controlled ventilation (VCV) and pressure-controlled ventilation (PCV) in pediatric patients with acute respiratory distress syndrome (ARDS).

DESIGN

Prospective cohort study.

SETTING

Seven-bed PICU, Hospital El Carmen de Maipú, Chile.

PATIENTS

Eighteen mechanically ventilated patients less than or equal to 15 years old undergoing neuromuscular blockade as part of management for ARDS.

INTERVENTIONS

None.

MEASUREMENTS AND MAIN RESULTS

All patients were in VCV mode during measurement of pulmonary mechanics, including: the first pressure drop (P1) upon reaching zero flow during the inspiratory hold, peak inspiratory pressure (PIP), plateau pressure (P PLAT ), and total positive end-expiratory pressure (tPEEP). We calculated the components of the working pressure, as defined by the following: frictional resistive = PIP-P1; viscoelastic resistive = P1-P PLAT ; purely elastic = driving pressure (ΔP) = P PLAT -tPEEP; and threshold = intrinsic PEEP. The procedures and calculations were repeated on PCV, keeping the same tidal volume and inspiratory time. Measurements in VCV were considered the gold standard. We performed Spearman correlation and Bland-Altman analysis. The median (interquartile range [IQR]) for patient age was 5 months (2-17 mo). Tidal volume was 5.7 mL/kg (5.3-6.1 mL/kg), PIP cm H 2 O 26 (23-27 cm H 2 O), P1 23 cm H 2 O (21-26 cm H 2 O), P PLAT 19 cm H 2 O (17-22 cm H 2 O), tPEEP 9 cm H 2 O (8-9 cm H 2 O), and ΔP 11 cm H 2 O (9-13 cm H 2 O) in VCV mode at baseline. There was a robust correlation (rho > 0.8) and agreement between frictional resistive, elastic, and threshold components of working pressure in both modes but not for the viscoelastic resistive component. The purely frictional resistive component was negligible. Median peak inspiratory flow with decelerating-flow was 21 (IQR, 15-26) and squared-shaped flow was 7 L/min (IQR, 6-10 L/min) ( p < 0.001).

CONCLUSIONS

P PLAT , ΔP, and tPEEP can guide clinical decisions independent of the ventilatory mode. The modest purely frictional resistive component emphasizes the relevance of maintaining the same safety limits, regardless of the selected ventilatory mode. Therefore, peak inspiratory flow should be studied as a mechanism of ventilator-induced lung injury in pediatric ARDS.

摘要

目的

研究急性呼吸窘迫综合征(ARDS)患儿在容量控制通气(VCV)和压力控制通气(PCV)期间的摩擦阻力、粘弹性阻力和弹性阻力成分以及阈值压力。

设计

前瞻性队列研究。

地点

智利马伊普市埃尔卡门医院有七张床位的儿科重症监护病房(PICU)。

患者

18例年龄小于或等于15岁的机械通气患者,作为ARDS治疗的一部分接受神经肌肉阻滞。

干预措施

无。

测量指标及主要结果

在测量肺力学指标期间,所有患者均处于VCV模式,这些指标包括:吸气末流量为零时的首次压力下降(P1)、吸气峰压(PIP)、平台压(P PLAT)和总呼气末正压(tPEEP)。我们计算了工作压力的组成部分,定义如下:摩擦阻力=PIP - P1;粘弹性阻力=P1 - P PLAT;纯弹性阻力=驱动压力(ΔP)=P PLAT - tPEEP;阈值=内源性PEEP。在PCV模式下重复上述步骤和计算,保持相同的潮气量和吸气时间。VCV模式下的测量被视为金标准。我们进行了Spearman相关性分析和Bland - Altman分析。患者年龄的中位数(四分位间距[IQR])为5个月(2 - 17个月)。潮气量为5.7 mL/kg(5.3 - 6.1 mL/kg),VCV模式下基线时PIP为26 cm H₂O(23 - 27 cm H₂O),P1为23 cm H₂O(21 - 26 cm H₂O),P PLAT为19 cm H₂O(17 - 22 cm H₂O),tPEEP为9 cm H₂O(8 - 9 cm H₂O),ΔP为11 cm H₂O(9 - 13 cm H₂O)。两种模式下工作压力的摩擦阻力、弹性阻力和阈值成分之间存在强相关性(rho > 0.8)和一致性,但粘弹性阻力成分除外。纯摩擦阻力成分可忽略不计。减速气流时的吸气峰流中位数为21(IQR,15 - 26),方波气流时为7 L/min(IQR,6 - 10 L/min)(p < 0.001)。

结论

P PLAT、ΔP和tPEEP可独立于通气模式指导临床决策。适度的纯摩擦阻力成分强调了无论选择何种通气模式,维持相同安全限度的相关性。因此,应将吸气峰流作为小儿ARDS中呼吸机诱导性肺损伤的一种机制进行研究。

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