Watremez Christine, Liistro Giuseppe, deKock Marc, Roeseler Jean, Clerbaux Thierry, Detry Bruno, Reynaert Marc, Gianello Pierre, Jolliet Philippe
Division of Anesthesiology, Clinique Universitaire St.-Luc, Brussels, Belgium.
Intensive Care Med. 2003 Sep;29(9):1560-6. doi: 10.1007/s00134-003-1779-y. Epub 2003 May 16.
To explore the consequences of helium/oxygen (He/O(2)) inhalation on respiratory mechanics, gas exchange, and ventilation-perfusion (VA/Q) relationships in an animal model of severe induced bronchospasm during mechanical ventilation.
Prospective, interventional study.
Experimental animal laboratory, university hospital.
Seven piglets were anesthetized, paralyzed, and mechanically ventilated, with all ventilator settings remaining constant throughout the protocol. Acute stable bronchospasm was obtained through continuous aerosolization of methacholine. Once steady-state was achieved, the animals successively breathed air/O(2) and He/O(2) (FIO(2) 0.3), or inversely, in random order. Measurements were taken at baseline, during bronchospasm, and after 30 min of He/O(2) inhalation.
Bronchospasm increased lung peak inspiratory pressure (49+/-6.9 vs 18+/-1 cm H(2)O, P<0.001), lung resistance (22.7+/-1.5 vs 6.8+/-1.5 cm H(2)O x l(-1).s, P<0.001), dynamic elastance (76+/-11.2 vs 22.8+/-4.1 cm H(2)O x l(-1), P<0.001), and work of breathing (1.51+/-0.26 vs 0.47+/-0.08, P<0.001). Arterial pH decreased (7.47+/-0.06 vs 7.32+/-0.06, P<0.001), PaCO(2) increased, and PaO(2) decreased. Multiple inert gas elimination showed an absence of shunt, substantial increases in perfusion to low VA/Q regions, and dispersion of VA/Q distribution. He/O(2) reduced lung resistance and work of breathing, and worsened hypercapnia and respiratory acidosis.
In this model, while He/O(2) improved respiratory mechanics and reduced work of breathing, hypercapnia and respiratory acidosis increased. Close attention should be paid to monitoring arterial blood gases when He/O(2) is used in mechanically ventilated acute severe asthma.
在机械通气期间严重诱导支气管痉挛的动物模型中,探讨氦氧(He/O₂)吸入对呼吸力学、气体交换和通气灌注(VA/Q)关系的影响。
前瞻性干预研究。
大学医院的实验动物实验室。
七只仔猪接受麻醉、麻痹并进行机械通气,在整个实验过程中所有通气设置保持不变。通过持续雾化乙酰甲胆碱诱导急性稳定的支气管痉挛。一旦达到稳态,动物依次随机呼吸空气/O₂和He/O₂(FIO₂ 0.3),或相反顺序。在基线、支气管痉挛期间以及He/O₂吸入30分钟后进行测量。
支气管痉挛使肺峰吸气压力升高(49±6.9 vs 18±1 cm H₂O,P<0.001)、肺阻力增加(22.7±1.5 vs 6.8±1.5 cm H₂O·l⁻¹·s,P<0.001)、动态弹性增加(76±11.2 vs 22.8±4.1 cm H₂O·l⁻¹,P<0.001)以及呼吸功增加(1.51±0.26 vs 0.47±0.08,P<0.001)。动脉pH降低(7.47±0.06 vs 7.32±0.06,P<0.001),PaCO₂升高,PaO₂降低。多惰性气体消除显示无分流,低VA/Q区域灌注显著增加,VA/Q分布离散。He/O₂降低了肺阻力和呼吸功,但使高碳酸血症和呼吸性酸中毒恶化。
在该模型中,虽然He/O₂改善了呼吸力学并降低了呼吸功,但高碳酸血症和呼吸性酸中毒加重。在机械通气的急性重症哮喘中使用He/O₂时,应密切关注监测动脉血气。