Krafft P, Fridrich P, Fitzgerald R D, Koc D, Steltzer H
Department of Anesthesiology and Intensive Care Medicine, University of Vienna, Austria.
Chest. 1996 Feb;109(2):486-93. doi: 10.1378/chest.109.2.486.
To evaluate the percentage of nitric oxide (NO) responders in septic shock patients with ARDS. Additionally, to investigate long-term NO effects on cardiac performance and oxygen kinetic patterns in NO responders vs nonresponders.
Prospective cohort study.
ICU of a university hospital.
Twenty-five consecutive patients with a diagnosis of septic shock and established ARDS requiring inotropic and vasopressor support.
After diagnosis of ARDS, NO was administered at 18 or 36 ppm. Patients demonstrating a NO-induced rise of arterial oxygen tension of 20% or more and/or a fall in mean pulmonary artery pressure of 15% or more were grouped as NO responders; others were grouped as nonresponders.
Ten patients (40%) were NO responders, while 15 patients (60%) were nonresponders. Mortality was 40% in NO responders and 67% in nonresponders (NS). NO responders developed a significantly lower mean pulmonary artery pressure (28 +/- 6 vs 33 +/- 6 mm Hg; p < 0.05), lower pulmonary vascular resistance (PVR: 258 +/- 73 vs 377 +/- 163 dyne.s.cm-5.m-2; p < 0.05), and higher PaO2/FIO2 ratio (192 +/- 85 vs 144 +/- 74 mm Hg; p < 0.05) within the study period. In responders, NO-induced afterload reduction resulted in increased right ventricular ejection fraction (RVEF: 40 +/- 7 vs 35 +/- 9%; p < 0.05), significantly higher cardiac index (CI: 4.5 +/- 1.1 vs 4.0 +/- 1.2 L.min-1.m-2; p < 0.05) and oxygen delivery (DO2: 681 +/- 141 vs 599 +/- 160 mL.min-1.m-2; p < 0.05) compared with nonresponders. In NO nonresponders, RVEF was correlated with PVR, CI, DO2, mixed venous oxygen saturation (SvO2), and oxygen extraction ratio (O2ER) (r = +/- 0.60 to +/- 0.69; p < 0.05). No significant correlation between RVEF and any of these parameters was observed in responders. SvO2 (75 +/- 7 vs 69 +/- 8%; p < 0.05) and O2ER (0.24 +/- 0.06 vs 0.27 +/- 0.06; p < 0.05) were significantly different between responders and nonresponders, while no difference in oxygen consumption was observed (161 +/- 41 vs 153 +/- 43 mL.min.m-2).
Inhaled NO is effective in only a subgroup of septic ARDS patients, with a higher, but insignificantly different percentage of survivors in the responder group. NO responders were characterized by increased RVEF accompanied by higher CI, DO2, and lower O2ER. In nonresponders, RVEF remained depressed, with a close correlation between RVEF and CO as well as DO2 and O2ER. Thus, nonresponders seem to suffer from impaired cardiac reserves and correspondingly lower oxygen transport variables.
评估急性呼吸窘迫综合征(ARDS)伴感染性休克患者中一氧化氮(NO)反应者的比例。此外,研究NO反应者与无反应者中,NO对心脏功能和氧动力学模式的长期影响。
前瞻性队列研究。
一所大学医院的重症监护病房(ICU)。
连续25例诊断为感染性休克且确诊为ARDS、需要使用血管活性药物支持的患者。
诊断ARDS后,给予18或36 ppm的NO。动脉血氧分压因NO诱导升高20%或更多和/或平均肺动脉压下降15%或更多的患者被归为NO反应者;其他患者归为无反应者。
10例患者(40%)为NO反应者,15例患者(60%)为无反应者。NO反应者的死亡率为40%,无反应者为67%(无统计学差异)。在研究期间,NO反应者的平均肺动脉压显著降低(28±6 vs 33±6 mmHg;p<0.05),肺血管阻力降低(PVR:258±73 vs 377±163 dyn·s·cm⁻⁵·m⁻²;p<0.05),动脉血氧分压/吸入氧分数比值升高(192±85 vs 144±74 mmHg;p<0.05)。在反应者中,NO诱导的后负荷降低导致右心室射血分数增加(RVEF:40±7 vs 35±9%;p<0.05),心脏指数显著升高(CI:4.5±1.1 vs 4.0±1.2 L·min⁻¹·m⁻²;p<0.05),氧输送增加(DO₂:681±141 vs 599±160 mL·min⁻¹·m⁻²;p<0.05)。在NO无反应者中,RVEF与PVR、CI、DO₂、混合静脉血氧饱和度(SvO₂)和氧摄取率(O₂ER)相关(r =±0.60至±0.69;p<0.05)。在反应者中未观察到RVEF与这些参数中的任何一个有显著相关性。反应者与无反应者之间的SvO₂(75±7 vs 69±8%;p<0.05)和O₂ER(0.24±0.06 vs 0.27±0.06;p<0.05)有显著差异,而氧消耗无差异(161±41 vs 153±43 mL·min·m⁻²)。
吸入NO仅对一部分感染性ARDS患者有效,反应者组的生存率较高,但差异无统计学意义。NO反应者的特征是RVEF增加,同时CI、DO₂升高,O₂ER降低。在无反应者中,RVEF仍然降低,RVEF与心输出量以及DO₂和O₂ER密切相关。因此,无反应者似乎存在心脏储备功能受损以及相应较低的氧输送变量。