Ballester E, Reyes A, Roca J, Guitart R, Wagner P D, Rodriguez-Roisin R
Department of Medicine, Hospital Clinic, University of Barcelona, Spain.
Thorax. 1989 Apr;44(4):258-67. doi: 10.1136/thx.44.4.258.
Ventilation-perfusion (VA/Q) relationships and gas exchange were studied by the multiple inert gas technique in 19 patients admitted to hospital with acute severe asthma (FEV1 41% predicted) before and during the administration of intravenous salbutamol, inhaled salbutamol, or 100% oxygen. Eight patients received a continuous intravenous infusion of salbutamol (4 micrograms/min, total dose 360 micrograms) and were studied before treatment, after 60 and 90 minutes of treatment, and one hour after treatment had been discontinued. Six patients had measurements before and 15 minutes after inhaling 300 micrograms salbutamol from a metered dose inhaler on two occasions (total dose 600 micrograms) and one hour after the last dose. Measurements were also made in five patients before and while they breathed 100% oxygen for 20 minutes. At baseline (fractional inspired oxygen (FiO2) 21%) all patients showed a broad unimodal (n = 10) or bimodal (n = 9) distribution of blood flow with respect to VA/Q. A mean of 10.5% of the blood flow was associated with low VA/Q units without any appreciable shunt. One of the best descriptors of VA/Q inequality, the second moment of the perfusion distribution on a log scale (log SD Q), was moderately high with a mean of 1.18 (SEM 0.08) (normal less than 0.6). Measures of VA/Q inequality correlated poorly with spirometric findings. After salbutamol the increase in airflow rates was similar regardless of the route of administration. Intravenous salbutamol, however, caused a significant increase in heart rate, cardiac output, and oxygen consumption (VO2); in addition, both perfusion to low VA/Q areas and log SD Q increased significantly. Inhaled salbutamol caused only minor changes in heart rate, cardiac output, VO2, and VA/Q inequality. Arterial oxygen tension (PaO2) remained unchanged during salbutamol administration, irrespective of the route of administration. During 100% oxygen breathing there was a significant increase in log SD Q (from 1.11 to 1.44). It is concluded that patients with acute severe asthma show considerable VA/Q inequality with a high level of pulmonary vascular reactivity. Despite similar bronchodilator effects from inhaled and intravenous salbutamol, VA/Q relationships worsened only during intravenous infusion. PaO2 remained unchanged, however, because the change in VA/Q relationships was associated with an increase in metabolic rate and cardiac output.
采用多惰性气体技术,对19例因急性重度哮喘入院的患者(预计第一秒用力呼气容积(FEV1)为41%)在静脉注射沙丁胺醇、吸入沙丁胺醇或吸入100%氧气前及过程中,研究其通气-灌注(VA/Q)关系及气体交换情况。8例患者接受沙丁胺醇持续静脉输注(4微克/分钟,总剂量360微克),分别在治疗前、治疗60分钟和90分钟后以及停药1小时后进行研究。6例患者在两次吸入定量气雾剂中300微克沙丁胺醇(总剂量600微克)前及吸入后15分钟以及最后一剂后1小时进行测量。还对5例患者在呼吸100%氧气20分钟前及过程中进行测量。在基线时(吸入氧分数(FiO2)为21%),所有患者的血流相对于VA/Q均呈现广泛的单峰(n = 10)或双峰(n = 9)分布。平均10.5%的血流与低VA/Q单位相关,无明显分流。VA/Q不均一性的最佳描述指标之一,即对数尺度下灌注分布的二阶矩(log SD Q),中度升高,平均值为1.18(标准误0.08)(正常小于0.6)。VA/Q不均一性指标与肺量计检查结果相关性较差。使用沙丁胺醇后,无论给药途径如何,气流速率的增加相似。然而,静脉注射沙丁胺醇导致心率、心输出量和氧耗量(VO2)显著增加;此外,低VA/Q区域的灌注及log SD Q均显著增加。吸入沙丁胺醇仅使心率、心输出量、VO2及VA/Q不均一性发生轻微变化。在使用沙丁胺醇期间,无论给药途径如何,动脉血氧张力(PaO2)均保持不变。在呼吸100%氧气期间,log SD Q显著增加(从1.11增至1.44)。结论是,急性重度哮喘患者存在相当程度的VA/Q不均一性及高水平的肺血管反应性。尽管吸入和静脉注射沙丁胺醇的支气管舒张作用相似,但仅在静脉输注期间VA/Q关系恶化。然而,PaO2保持不变,因为VA/Q关系的变化与代谢率和心输出量增加有关。