地塞米松对淡水淹溺型兔肺损伤血清NO的影响

目的观察淡水淹溺型兔肺损伤中NO的变化及地塞米松的干预作用。方法将21只大白兔随机分为空白对照组、淡水淹溺组、地塞米松治疗组。气管淡水灌注后于0、0.5、1、2、3、6 h抽血观察PaO2、PaCO2和NO变化,试验终点测定肺组织中丙二醛（MDA）、一氧化氮合酶（NOS）、超氧化物歧化酶（SOD）的含量变化。光镜下观察肺组织。结果淡水灌注后动物PaO2、PaCO2低,血清NO增高（P〈0.01）。肺组织中NOS、MDA含量增高（P〈0.01）,SOD降低（P〈0.05）。病理学显示淡水淹溺后出现肺间质、肺泡水肿及肺泡腔内炎性细胞浸润。地塞米松可减轻肺损伤。结论淡水淹溺可升高兔血清中NO;地塞米松可减轻淹溺后肺损伤。     

Enhancement of hypoxic pulmonary vasoconstriction by almitrine in the dog

In order to test the hypothesis of enhancement of hypoxic pulmonary vasoconstriction by Almitrine, 12 anesthetized and paralyzed dogs with normal lungs were studied under controlled ventilation. They were ventilated in random sequence with air, 12% O2, and 100% O2, and almitrine (0.1 mg/kg body weight) was infused over 30 min during each O2 mixture. The multiple inert gas elimination technique was used to detect alterations in ventilation-perfusion (VA/Q) mismatching before and during the interventions and to measure cardiac output (QT). Arterial, mixed venous and expired gases, inert gas concentrations, and hemodynamic measurements were made while the dogs were breathing the different O2 mixtures before infusing the drug, near the end of 30 min of infusion and 30 min after infusion had ended. There were no significant changes in pH, PaO2, PaCO2, QT, oxygen uptake, oxygen delivery index, systemic vascular resistance, mean systemic arterial pressure, heart rate, stroke volume index, or VA/Q distribution during the experiment. Significant increases in: (a) pulmonary artery pressure (PA), (b) the pressure difference between PA and pulmonary capillary wedge pressure (PCw), and (c) pulmonary vascular resistance (PVR) occurred when the drug was infused during 12% O2 and air, but not during 100% O2. The PVR increased 59.7% with almitrine infusion during 12% O2 and 38.4% during air breathing (p less than or equal to 0.01), but there was no significant change during 100% O2. Vascular responses were not dependent on the order in which the different O2 mixtures were administered. These data strongly suggest that almitrine enhances hypoxic vasoconstriction in the lung, and this effect may explain reported improvement in PaO2 in hypoxic patients given the drug.     

舒利迭吸入治疗AECOPD的临床观察

目的 观察舒利迭粉吸入剂(丙酸氟替卡松500 μg/沙美特罗50 μg)治疗AECOPD的疗效和安全性.方法 将74例住院AECOPD患者随机分为治疗组和对照组.对照组给予常规治疗,治疗组在此基础上给予舒利迭吸入,两组疗程均为10天.观察两组患者治疗后肺功能、血气、糖化血红蛋白(HbA1c)、8 AM空腹血糖(8AMFBG)及餐后2 h血糖(2 h PG)的变化.结果 两组FEV1/FVC、FEV1%预计值、PaO2分别较治疗前明显升高,差异有统计学意义(P＜0.05);治疗后治疗组FEV1/FVC、FEV1%预计值分别高于对照组,差异有统计学意义(P<0.05).两组PaCO2较治疗前明显下降,差异有统计学意义(P＜0.05);治疗后治疗组PaCO2较对照组下降显著,差异有统计学意义(P<0.05).两组治疗前后HbA1c、8AMFBG及2 h PG的差异不明显,无统计学意义(P>0.05).结论 舒利迭粉吸入是治疗AECOPD安全有效的方法.     

Pulmonary hemodynamics and gas exchange during exercise in liver cirrhosis

We have recently shown that ventilation-perfusion (VA/Q) mismatching at rest in cirrhosis is due to an abnormal pulmonary vascular tone. It has been suggested that in patients with cirrhosis, O2 transfer might become diffusion-limited during exercise. This study examined pulmonary hemodynamics and mechanisms modulating gas exchange during exercise (60 to 70% VO2max) in six patients (41 +/- 5 yr, mean +/- SEM) with cirrhosis but with normal lung function tests. At rest, QT was high (8.4 +/- 0.5 L/min), pulmonary vascular resistance (PVR) was low (0.61 +/- 0.17 mm Hg/L/min), and there was mild to moderate VA/Q mismatching (LogSD Q, 0.79 +/- 0.09; normal range, 0.3 to 0.6). However, hyperventilation (PaCO2, 29 +/- 2 mm Hg) and high QT (thus, high PVO2, 41 +/- 2 mm Hg) contributed to the maintenance of PaO2 within normal values (99 +/- 7 mm Hg). Exercise VO2 (1,278 +/- 122 ml/min) was normal relative to work load, but, contrary to that in normal subjects, QT was higher and PVR did not fall. During exercise, PaO2 showed a trend to decrease (to 90 +/- 5 mm Hg) and PaCO2 to rise (to 35 +/- 2 mm Hg), but the differences failed to reach statistical significance (p = 0.07 each). PVO2 fell significantly with exercise (41 +/- 2 to 33 +/- 0.3 mm Hg, p less than 0.05), but neither AaPO2 (15 +/- 7 to 21 +/- 6 mm Hg) nor VA/Q inequality (LogSD Q, 0.82 +/- 0.11) changed. No systemic difference was noticed between predicted and measured PaO2 values, suggesting no O2 diffusion impairment during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gas exchange and pulmonary vascular reactivity in patients with liver cirrhosis

To investigate the mechanisms underlying abnormal gas exchange in liver cirrhosis, 15 patients were studied while breathing room air, 11% O2, and 100% O2 in random sequence. Under basal conditions, patients showed mild reductions from normal in systemic and pulmonary vascular resistance, normal PaO2 (mean, 92.5 +/- 2.5 mm Hg), mild hypocapnia (mean, 34 +/- 0.7 mm Hg), and a slightly right-shifted oxyhemoglobin dissociation curve (P50, 27.2 +/- 0.4 mm Hg; 2,3-DPG, 13.1 +/- 0.6 mumol/g). Using the multiple insert gas elimination technique, we found mild to moderate ventilation-perfusion (VA/Q) inequality with a mean of 5% (range, 0 to 20%) of cardiac output (QT) perfusing low VA/Q ratio (less than 0.1) areas but no shunt. Breathing 11% O2, there were significant increases in QT, pulmonary artery pressure, and vascular resistance, whereas no changes occurred in VA/Q distribution, and there was no evidence for alveolar-endcapillary diffusion limitation for O2. In contrast, after 100% O2 shunt developed and VA/Q relationships worsened without significant hemodynamic changes. Furthermore, patients with cutaneous spider nevi (n = 8) showed more hepatocellular dysfunction (lower prothrombin values), lower systemic and pulmonary vascular resistance, less hypoxic pulmonary vasoconstriction (HPV), lower PaO2, and more VA/Q mismatch than did those without spiders. Our results confirm, therefore, that HPV is not fully abolished, as previously described, in hepatic cirrhosis. However, those patients with more advanced hepatic disease exhibit inadequate pulmonary vascular tone, which increases VA/Q inequality and lowers PaO2.     

Ventilation-perfusion distributions and central hemodynamics in chronic obstructive pulmonary disease. Effects of terbutaline administration

We studied the effects of intravenous terbutaline on VA/Q distributions and central hemodynamics in 11 patients with mixed-type COPD. Terbutaline caused an increase in VA/Q inequality in patients having PaO2 values greater than 60 mm Hg which resulted in a moderate fall in the PaO2. Patients with PaO2 values less than 60 mm Hg, the highest mean PAPs and the poorest spirometric performances demonstrated no significant changes in VA/Q distributions or PaO2 after terbutaline. Cardiac output increased 40 to 60 percent in all patients after terbutaline with an increase in tissue oxygen delivery. Mean PAP did not change in any patient after terbutaline and pulmonary vasodilatation was indicated by a decrease of calculated static PVR. The decrease of PaO2 after terbutaline in COPD is related to a further deterioration of existing VA/Q relationships. The cause of these effects and lack of such responses in patients with more advanced disease are discussed.     

Effect of almitrine in acute canine lung injury induced by paraquat]

The effects of intravenously administered almitrine (0.3 or 1.0 micrograms/kg/min, for 30 min) on hemodynamics and pulmonary gas exchange were assessed in eight dogs with acute lung injury induced by paraquat under controlled ventilation. Arterial blood gases, pulmonary and systemic hemodynamics, and ventilation-perfusion distribution (VA/Q) using the multiple inert gas elimination technique were examined before (control) and during infusion of almitrine. Almitrine produced significant increases in mean pulmonary arterial pressure from 17.4 +/- 3.3 (control, mean +/- SD) to 20.4 +/- 1.5 mmHg (1.0 micrograms/kg/min), and in total pulmonary vascular resistance. There was no change in other hemodynamic parameters, arterial gas tensions, or VA/Q distribution. These results indicate that almitrine causes pulmonary vasoconstriction without changing ventilation-perfusion distribution in dogs with paraquat-induced lung injury.     

The relationship between pulmonary function tests, thorax HRCT, and quantitative ventilation-perfusion scintigraphy in chronic obstructive pulmonary disease

We have evaluated the relationship between pulmonary function tests (PFT), thorax high resolution computed tomography (HRCT) images and quantitative ventilation-perfusion (V/Q) scintigraphic studies in 16 male patients (mean age 65.6 +/- 5.5 years) with chronic obstructive pulmonary disease (COPD). The mean forced vital capacity (FVC) value of the patient group was 2352 +/- 642 mL (65.4 +/- 15.8%), whereas mean forced expiratory volume in one second (FEV(1)) was found to be 1150 +/- 442 mL (40.8 +/- 14.9%). The ratio of carbon monoxide diffusion capacity to alveolar ventilation (DLCO/VA) was 3.17 +/- 0.88 mL/min/mmHg/L, and the mean partial oxygen (PaO(2)) and carbon dioxide (PaCO(2)) pressures were 68.5 +/- 11.04 mmHg and 38.9 +/- 5.8 mmHg respectively. For each patient, thorax HRCT and V/Q scintigraphic images of both lungs were divided into upper, mid and lower zones during examination. Visual scoring for the assessment of emphysema on thorax HRCT were used and images were graded from mild to severe (< or = 25% - > or = 76%). Emphysema scores were found to be higher on upper zones with accompanying lowest V/Q ratios. DLCO/VA, DLCO, total emphysema scores, and individual emphysema scores of the upper, mid and lower zones were found to be correlated. As a conclusion, it can be stated that emphysematous changes in COPD patients are more apparent in the upper lung zones, which also have the lowest V/Q ratios.     

Comparison of arterial-end-tidal PCO2 difference and dead space/tidal volume ratio in respiratory failure

End-tidal CO2 monitors are used to estimate arterial CO2 pressure (PaCO2), but appropriate use of this noninvasive method of assessing blood gases is unclear. In patients with lung disease, the end-tidal CO2 pressure (PETCO2) can differ from PaCO2 because of ventilation-perfusion (VA/Q) mismatching, and changes in PETCO2 may be seen with corresponding increase, decrease, or no change in PaCO2 depending on what happens to VA/Q mismatching. We compared the difference between PETCO2 and PaCO2 in 17 patients undergoing mechanical ventilation. Large differences were found between PaCO2 and PETCO2 in individual patients; P(a-et)CO2 correlated closely with VD/VT. Our studies confirm that PetCO2 is a poor estimate of PaCO2 in patients with respiratory failure. However, the P(a-et)CO2 may be the most appropriate use for end-tidal PCO2 monitoring. In addition, we found that the end-tidal CO2 monitor may be easily adapted for expedient measurement of VD/VT.     

Arterial oxygenation and pulmonary function with Saralasin in chronic lung disease

During our earlier saralasin infusion study in hypertensive patients, we found a drug-induced rise in arterial oxygen tension (PaO2) associated with unchanged mixed venous PO2 or the PaCO2 and unrelated to cardiopulmonary hemodynamic changes. To test the hypothesis that saralasin improved pulmonary mechanics, blood gases, lung mechanics, lung volumes, diffusing capacity, and distribution of ventilation were analyzed and cardiac output (CO) measured in 12 normotensive men with chronic pulmonary disease before and during a 2 1/2 hour infusion of Saralasin (5 micrograms/kg/min). The PaO2 increased from a mean of 63 +/- 3 (SEM) to 70 +/- 3 mm Hg (p less than 0.001), while the CO decreased from 6.81 +/- 0.52 L/min to 6.18 +/- 0.48 L/min (p less than 0.005). The change in (delta)CO correlated with delta PaO2 (r = -0.67, p less than 0.05). Total systemic vascular resistance rose from 1,201 +/- 134 to 1,353 +/- 147 dynes X sec X cm5 (p less than 0.001). The PaCO2 and other measurements remained unchanged. We conclude that saralasin raised the PaO2 not by changing pulmonary function or mechanics, but by redistributing pulmonary blood flow and improving the ventilation-perfusion relationship.     

Effect of almitrine on ventilation-perfusion distribution in adult respiratory distress syndrome

Almitrine improves ventilation/perfusion relationships (VA/Q) in COPD, but its effects in ARDS, in which VA/Q mismatching is the cause of severe hypoxemia, are not known. The effects of almitrine on pulmonary gas exchange and circulation were assessed in 9 patients with ARDS who were sedated, paralyzed, and mechanically ventilated at constant FlO2 (range, 0.48 to 0.74). Systemic and pulmonary hemodynamics, conventional gas exchange, and the VA/Q distribution by the multiple inert gas elimination technique (MIGT) were measured before (baseline), during (ALM 15), at the end of (ALM 30), and at 30-min intervals after (POSTALM 30, 60, and 90) the intravenous infusion of 0.5 mg/kg body weight of almitrine over 30 min. Almitrine significantly increased PaO2 from 78 +/- 15 mm Hg to 140 +/- 49 at ALM 15 and 138 +/- 52 at ALM 30. AaPO2 and QS/QT decreased during the administration of the drug. The MIGT showed that almitrine redistributed pulmonary blood flow from shunt areas (reduction from 29 +/- 11 to 17 +/- 11% of QT) to lung units with normal VA/Q ratios (increase from 63 +/- 9 to 73 +/- 6% of QT). The Ppa increased from 26 +/- 5 to 30 +/- 5 mm Hg without changes in QT. Changes were transient, returning toward baseline 30 min after stopping the infusion of the drug. Almitrine significantly reduced the VA/Q inequalities present in ARDS and may be useful in the management of those patients.     

重症急性胰腺炎致急性肺损伤动物模型血气分析及形态学研究

目的观察sD大鼠重症急性胰腺炎致急性肺损伤后动脉血气分析及形态学改变。方法健康成年sD大鼠20只,随机分成两组,A组10只,注射同等剂量的生理盐水;B组10只,腹腔注射脂多糖建立重症急性胰腺炎的动物模型,观察病理学改变。结果血气分析变化：①PaO2：伤后12～48h两组sD大鼠相比较有差异（P〈0．05）,B组低于A组。②PaCO2：两组SD大鼠伤后12～48h相比较均有差异（P〈0．01）,B组高于A组。病理学改变：B组急性肺损伤表现（中性粒细胞浸润、肺泡内炎性物质渗出）,随着时间延长,视野内中性粒细胞增多。结论动脉血气指标PaO2、PaCO2在重症急性胰腺炎致急性肺损伤后可用作为判断肺组织损伤严重程度的参考指标,PaO2水平能反映肺损伤程度,在伤后24h～48h检测的指标更明显。     

Improvement in ventilation-perfusion relationships by almitrine in patients with chronic obstructive pulmonary disease during mechanical ventilation

Although the respiratory stimulant effects of almitrine bismesylate (AB) via an action on the peripheral chemoreceptors have been demonstrated, the mechanism of its intrapulmonary action has not yet been elucidated. In order to abolish the stimulation of ventilation, observed in studies on spontaneously breathing patients, an investigation of patients suffering from severe COPD under constant mechanical ventilation, with FIO2 = 0.21, during the weaning period was carried out. Eighteen patients were randomly divided into 2 groups (9 receiving 1.5 mg/kg AB and 9 receiving placebo). The ventilatory and hemodynamic variables, blood and alveolar gases, and the VA/Q ratio distributions using the multiple inert gas technique were collected before treatment with drug or placebo, as well as 90 and 180 min afterwards. The PaO2 was found to be raised 90 min after AB administration (+57 +/- 3.9 mm Hg, p less than 0.01) and remained above the baseline value at 180 min (+5.4 +/- 4.6 mm Hg, p less than 0.01). Compared with those in the placebo group, these increases were significant (p less than 0.01). A slight decrease in PaCO2 but similar in the 2 groups was observed despite constant ventilation. The hemodynamic data were the same for the 2 groups. The changes in overall criteria of the distributions (mean VA/Q and SD) were small. The main finding was a decrease in the percentage of the perfusion flowing through the true shunt and the underventilated areas after AB treatment. In the control group, the blood flow percentage in the true shunt and low VA/Q units was either stable or increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Tiotropium is less likely to induce oxygen desaturation in stable COPD patients compared to long-acting beta2-agonists

In a three-way crossover pilot study, the acute effects of tiotropium 18 microg inhalation on the respiratory function and arterial blood gas tensions of 30 patients with stable chronic obstructive pulmonary disease (COPD) were compared with those of salmeterol 50 microg and formoterol 12 microg. In each study day, lung function and arterial blood gas analyses were performed before and up to 180 min after inhalation. All treatments significantly improved lung function, increased DLco, decreased PaO2, and increased P(A-a)O2, with no change in PaCO2. The effects of salmeterol and tiotropium on PaO2 were slower in onset and more prolonged than those of formoterol but PaO2AUC0-180 min was significantly greater for formoterol and salmeterol than for tiotropium. It is likely that the significant but small decreases in PaO2 and increases in P(A-a)O2 have been caused by pulmonary vasodilator effects. Since the three agents were similar in inducing bronchodilation, we believe that tiotropium is preferable in patients with hypoxemia caused by stable COPD because it seems to carry a smaller risk of worsening systemic hypoxemia.     

Uneven ventilation-perfusion ratio distribution during acute exacerbation of chronic pulmonary diseases]

We studied ventilation-perfusion ratio (VA/Q) unevenness in terms of alveolar-arterial gas tension difference (AaDO2 and aADN2) and of multiple inert gas elimination technique during the chronic stable periods and the acute exacerbation periods of seven cases with chronic pulmonary diseases. Three had idiopathic pulmonary fibrosis, 2 had pulmonary emphysema, 1 had bronchiolitis and the other had a sequelae of pulmonary tuberculosis. Sulfur hexafluoride and cyclopropane dissolved in saline were infused into a peripheral vein at a constant rate and these 2 gases were used as the indicator gases to make analysis of two compartmental VA/Q. During exacerbation all cases showed lower PaO2 than in the stable period. All cases except idiopathic pulmonary fibrosis showed higher PaCO2. Five cases also had higher AaDO2 and aADN2. One case with pulmonary emphysema and one with bronchiolitis actually had lower AaDO2 and aADN2 values during acute exacerbation than during the chronic stable period. We introduced the difference between the logarithm of higher VA/Q and lower VA/Q values (log [(VA/Q)H/(VA/Q)L)] as an index of VA/Q unevenness. Two compartmental VA/Q analysis revealed greater VA/Q differences in all cases during acute exacerbation. This included cases who showed lower AaDO2 and aADN2 values in the acute exacerbation period. In conclusion, worsened VA/Q distribution, during the acute exacerbation period, was elucidated quantitatively using the multiple inert gas elimination technique.     

Ventilation-perfusion inequality in patients with non-alcoholic liver cirrhosis

Ventilation-perfusion relationships were studied in patients with non-alcoholic liver cirrhosis. Spirometry was essentially normal but the transfer factor of the lung (DLCO) was reduced by an average 34% of predicted. Arterial oxygen tension (PaO2) ranged from normal down to 6.9 kPa. Varying degrees of ventilation-perfusion (VA/Q) abnormalities (multiple inert gas elimination technique) were observed with increased dispersion of the perfusion distribution (log SDQ, 0.90; range 0.32-1.71; upper normal limit, 0.60) and the presence of both regions of low VA/Q ratios (between 0.1 and 0.005) (mean 4.1%; range 0-18.8%) and shunt (VA/Q ratios below 0.005) (mean 3.9%; range 0.19.8%). There was a close similarity between measured and calculated PaO2 in normoxaemic patients, but calculated values exceeded measured PaO2 in hypoxaemic patients. The difference between calculated and measured PaO2 correlated inversely to DLCO (r = 0.65, p less than 0.05). An inverse correlation was also noted between DLCO and the sum of shunt and low VA/Q regions (r = 0.87, p less than 0.001). It is concluded that hypoxaemia in non-alcoholic liver cirrhosis patients can be accounted for by intrapulmonary shunting and VA/Q mismatch, and possibly a "diffusion-perfusion" defect in patients with more severe gas exchange impairment.     

常规应用乌司他丁联合复方丹参注射液对百草枯中毒患者肺损伤的疗效观察

目的探究常规应用乌司他丁联合复方丹参注射液对百草枯中毒患者肺损伤的疗效。方法选取2010年7月至2013年7月来我院就诊的100例百草枯中毒患者,依据分层随机分组法将患者分为治疗组和对照组,每组50例。对照组给予积极的常规疗法及丹参注射液进行治疗,治疗组在常规治疗的基础上加用乌司他丁联合复方丹参注射液治疗。分别于治疗前及治疗2周后检测PaO2、PaCO2及氧合指数,观察紫绀例数及ARDS发生例数,并于治疗前及治疗后1周、2周及4周检测患者的血清血红素氧合酶-1。结果治疗前两组检测指标差异无统计学意义;治疗2周后治疗组的PaO2、PaCO2、氧合指数及血红素氧合酶1明显高于对照组（t值分别为3．520、2．597、2.425、2．197,P值均〈0．05）,治疗组患者的紫绀及ARDS发生率均低于对照组（X^2值分别为5．316、4．971,P值均〈0．05）。结论百草枯中毒患者常规治疗基础上应用乌司他丁联合复方丹参注射液治疗可明显改善患者肺损伤指标,促进患者的损伤修复,建议临床积极推广。     

Severe hypoxemia and liver disease

Severe hypoxemia and orthodeoxia in patients with chronic liver disease is uncommon, but, when present, it is incapacitating. The purpose of this study was to determine the distribution of alveolar ventilation-perfusion (VA/Q) in six patients with mild liver disease and severe hypoxemia (PaO2 at rest in sitting or standing position ranged from 35 to 67 mm Hg). Orthodeoxia was documented with improvement in PaO2 in the supine position in each patient (PaO2 at rest in supine position ranged from 46 to 75 mm Hg). VA/Q distribution was measured by the multiple inert gas elimination technique. The dispersion of VA/Q was increased with small portions of the cardiac output (0.5 to 14.8%) perfusing low VA/Q areas (O less than VA/Q less than 0.1). Another major finding was a large right-to-left shunt (VA/Q less than 0.005) that ranged from 4 to 28%. The VA/Q mismatching and the right-to-left shunt both contributed to the hypoxemia. The predicted PaO2 was 5.5 mm Hg (p less than 0.01) larger than the measured PaO2. In each patient, the mean pulmonary artery pressure was low and the cardiac output was elevated. These results show that the low PaO2 in these patients was due to both increased right-to-left shunt and VA/Q mismatching, but impaired diffusion could not be ruled out.     

The metabolic index of nocturnal hypoxia in patients after lung resection and thoracoplasty

The authors measured urinary uric acid (UA) and creatinine (CR), serum lactate, and CoQ10 prior to retiring at night and on awakening in the morning in 127 patients (PG) after lung resection and thoracoplasty which were done more than 20 years age for treatment of tuberculosis and in 20 controls (NC). delta UA:CR, delta lactate, and delta CoQ10 were calculated respectively as the overnight changes in urinary UA:CR and in serum lactate and CoQ10. delta UA:CR increased in PG (4.0 +/- 43.6%), whereas it decreased in NC (-22.3 +/- 17.7%) (mean +/- SD) (p less than 0.05). Nocturnal hypoxemia suggested from positive balance of delta UA:CR was seen in 37% of PG, but in only 10% of NC. delta UA:CR showed no relationship with delta lactate and delta CoQ10 and also did not correlate with the nadir of arterial oxygen saturation. PG were divided into PG with a positive balance of delta UA:CR (PG-P) and with a negative balance of delta UA:CR (PG-N). The %VC and PaO2 in the PG-P group were lower and PaCO2 was higher than in PG-N, although the difference did not achieve statistical significance.     

Mechanisms of hypoxemia in patients with status asthmaticus requiring mechanical ventilation

Eight consecutive patients (mean +/- SD age, 43 +/- 11 yr) with acute severe asthma (status asthmaticus) requiring assisted ventilation were studied within the first 24 to 48 h of admission, at maintenance FIO2 and while breathing 100% O2, using the multiple inert gas elimination technique. Ventilation-perfusion (VA/Q) inequality was characterized by a marked bimodal blood flow distribution (perfusion to normal and low VA/Q populations) in all but two patients, with a mean of 27.6 +/- 12.3% of the total perfusion present in the low VA/Q ratio units (between 0.1 and 0.005). As a result, the dispersion of pulmonary blood flow distribution (log SDQ) was severely abnormal (mean, 1.65 +/- 0.28; normal range, 0.3 to 0.6). No patient had a substantial shunt (VA/Q = 0) (mean value, 1.5 +/- 2.3%). The ventilation distribution was never bimodal, but the dispersion of the ventilation distribution (log SDV) was moderately elevated (1.01 +/- 0.24). High VA/Q areas (ventilation to VA/Q units between 10 and 100) were generally absent. While breathing 100% O2, PaO2, PvO2, and PaCO2 significantly rose, as did shunt and blood flow dispersion. Patients with life-threatening acute severe asthma treated by mechanical ventilation show: (1) the most abnormal gas exchange characteristics of the VA/Q spectrum observed to date in human asthma but essentially the same pattern as in patients with less severe disease; (2) a high level of hypoxic pulmonary vascular response; (3) a significant amount of shunt while breathing 100% O2, suggesting the presence of absorption atelectasis or redistribution of blood flow.