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Ventilation-perfusion mismatching in acute severe asthma: effects of salbutamol and 100 oxygen.

机译:急性严重哮喘中的通气-灌注不匹配:沙丁胺醇和100%氧气的作用。

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摘要

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.
机译:通过多惰性气体技术研究了在静脉注射沙丁胺醇,吸入沙丁胺醇或100例急性重度哮喘(预测FEV1为41%)住院的19例患者中的通气-灌注(VA / Q)关系和气体交换%氧气。八名患者接受了沙丁胺醇的连续静脉滴注(4微克/分钟,总剂量360微克),并在治疗前,治疗60和90分钟后以及停药一小时后进行了研究。六例患者在两次(总剂量为600微克)吸入后从计量吸入器中吸入300毫克沙丁胺醇之前和之后的一小时和15分钟后进行了测量。还对五名患者在呼吸100%氧气20分钟之前和之时进行了测量。在基线时(分数吸入氧气(FiO2)为21%),所有患者相对于VA / Q表现出较宽的单峰(n = 10)或双峰(n = 9)血流分布。平均10.5%的血流与低VA / Q单位有关,而没有任何明显的分流。 VA / Q不平等的最佳描述者之一是对数标度上的灌注分布的第二时刻(log SD Q)中等偏高,平均值为1.18(SEM 0.08)(通常小于0.6)。 VA / Q不平等的量度与肺活量测定结果的相关性很差。沙丁胺醇给药后,无论给药途径如何,气流速率的增加都是相似的。但是,静脉注射沙丁胺醇会导致心率,心输出量和氧气消耗量(VO2)显着增加。此外,低VA / Q区域的灌注和log SD Q均显着增加。吸入沙丁胺醇只会引起心率,心输出量,VO2和VA / Q不平等的轻微变化。沙丁胺醇给药期间的动脉血氧分压(PaO2)保持不变,与给药途径无关。在进行100%的氧气呼吸期间,log SD Q显着增加(从1.11增至1.44)。结论是,急性严重哮喘患者表现出相当大的VA / Q不平等,并且肺血管反应性很高。尽管吸入和静脉给予沙丁胺醇具有类似的支气管扩张剂作用,但VA / Q关系仅在静脉输注期间恶化。 PaO2保持不变,但是,因为VA / Q关系的改变与代谢率和心输出量的增加有关。

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