23例肝肺综合征临床分析

探讨肝肺综合征(HPS)的临床特点和预后。67例肝硬化患者均应用血气分析仪测定其动脉血氧分压(PaO2),其中Ch ild-Pugh分级A级30例,B级22例,C级15例。67例肝硬化患者中23例合并HPS,发病率为34.3%。其发病率与Ch ild-Pugh分级有关,与A级比较C级HPS,发病率显著增高(P<0.05);门静脉增宽与不宽者、胃底食管静脉曲张与未发现曲张者、有蜘蛛痣与无蜘蛛痣者分别合并有HPS,两者比较均差异有显著性(P<0.05)。23例HPS患者中7例死亡,HPS均不是直接死亡原因。有门脉高压、蜘蛛痣时提示HPS的存在。早期诊断和治疗有助于缓解低氧血症,改善预后。     

Effects of buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (Paco_2-20 kPa) at Fio₂ 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 ±0.01 vs 7.01±0.01 (mean ± s.e.mean, P < 0.01). Serum osmolality and Paco₂ did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 ± 6 vs 189±12 min^-1 (P < 0.01), mean arterial pressure (MAP) 109 ± 4 vs 124 ± 4 mmHg (14.5 ± 0.5 vs 16.5 ± 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16±1 vs 23 ± 1 mmHg (2.1 ±0.1 vs 3.1 ±0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 ± 21 vs 343 ± 20 dyn s-cm^-5 (2490±210 vs 3430±200 μN-s-cm^-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in Fio₂ (0.15, 0.10, 0.05) at 30-min intervals, while Fico₂ was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At Fio₂ 0.15, buffered animals had higher arterial oxygen saturation (73 ± 5%) than the controls (55 ± 5%), (P < 0.05). The control animals died after 1–29 min (mean 14 min) at Fio₂ 0.10, while all buffered animals survived Fio₂ 0.10 with stable MAP (122 ± 14 mmHg (16.3 ± 1.9 kPa). The buffered animals died after 4–22 min (mean 15 min) at Fio₂ 0.05. We conclude that buffering to a pH of 7.21 attenuates the observed hemodynamic response in extreme hypercapnia and improves survival in hypercapnic hypoxemia.     

矽肺患者肺功能与动脉血气分析的研究

本文对88例矽肺病人和37名接尘工人进行了肺功能和动脉血气分析,结果表明各期矽肺的VC、FVC、FEV_1、MMF、FEV_1/FVC均值低于接尘组,而异常检出率则高于接尘组,通气功能的下降呈进行性,但早期不很明显,与接尘组无显著差异。各期矽肺组V_(50)及V_(25)均有明显降低,显示早期即有小气道的广泛损害。矽肺的通气功能损害类型,Ⅰ期矽肺组以阻塞型多见,Ⅱ、Ⅲ期矽肺组以混合型为主。RV和RV/TLC在Ⅲ期矽肺组有明显增高,表明矽肺晚期多并发肺气肿。另外DL_(CD)和K_(CD)在各矽肺组均低于接尘组,差异有显著性,说明矽肺早期即可有弥散功能的损害。血气分析表明PaO_2及SatO_2降低主要见于Ⅱ、Ⅲ期矽肺。Ⅲ期矽肺组有1/3患者(33.33％)在有低氧血症的同时合并有高碳酸血症。对比肺功能和血气分析结果,认为通气功能指标FEV_1、FEV_1/FVC、VC、FVC、MMF以及弥散功能指标DL_(CO)和K_(CO)为早期反映矽肺呼吸功能的灵敏指标。血气分析对病情和预后的判断有重要参考价值。     

Poor oxygenation in the lungs of patients with hyperosmolar hyperglycemic non-ketotic diabetic coma after cardiac surgery

The ratio of PaO₂ to FiO₂ was often low (300 or less) in four patients with complications of hyperosmolar hyperglycemic non-ketotic diabetic coma (HHNKDC) following open heart surgery. Four of our patients had poor oxygenation and subsequent spontaneous recovery from in the immediate post-operative period, although HHNKDC occurred only in one during this period. In the 3 others, poor oxygenation without accompanying HHNKDC lasted for 1–6 days and HHNKDC developed about 2 weeks after open heart surgery at time when poor oxygenation reoccurred. If a working diagnosis of congestive heart failure was made only on the basis of the most common probability, and the fluid supply was restricted, HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced. It is thus concluded that HHNKDC should be included in diagnoses for pulmonary dysfunction.     

Comparative effects of ischemia and acute hypoxemia on muscle afferents from tibialis anterior in cats

Comparative effects of ischemia and acute hypoxemia (PaO₂ = 24 mm Hg) were studied in anesthetized cats on afferents from the tibialis anterior limb muscle. Metaboreceptors (groups III and IV fibers) and mechanoreceptors were identified by their activation by an intraarterial injection of lactic acid (LA) or high-frequency vibrations (HFV) applied to the extremity of the muscle tendon, respectively. Ischemia and hypoxemia exerted opposite influences on the two categories of muscle afferents: they depressed the response of mechanoreceptors to HFV, but markedly enhanced the spontaneous tonic activity of metaboreceptors. The effects of hypoxamia were delayed but slightly greater and lasted longer during the recovery period than those exerted by ischemia. The inhibitory action on mechanoreceptors exerted by a reduced oxyden supply to muscle is interpreted as a result from local acidosis. Indeed, under normoxic conditions, a LA bolus injection during the HFV test also reduced the firing rate of these receptors. © 1993 John Wiley & Sons, Inc.     

Effects of reduced frequency breathing on arterial hypoxemia during exercise

Summary It is uncertain that exercise with reduced frequency breathing (RFB) results in arterial hypoxemia. This study was designed to investigate whether RFB during exercise creates a true hypoxic condition in arterial blood by examining arterial oxygen saturation (SaO₂) directly. Six subjects performed ten 30 s periods of exercise on a Monark bicycle ergometer at a work rate of 210 W alternating with 30 s rest intervals. The breath was controlled to use 1 s each for inspiration and expiration, and two trials with different breathing patterns were used; a continuous breathing (CB) trial and an RFB trial consisting of four seconds of breath-holding at functional residual capacity (FRC). Alveolar oxygen pressure during exercise showed a slight but significant (p<0.05) reduction with RFB as compared to CB. However, a marked increase in alveolar-arterial pressure difference for oxygen (A-aDO₂) (p<0.05) with RFB over CB resulted in a marked (p<0.05) reduction in arterial oxygen pressure. Consequently, SaO₂ fell as low as 88.8% on average. Additional examination of RFB with breath-holding at total lung capacity showed no increases in A-aDO₂ in spite of the same amount of hypoventilation as compared with that at FRC. These results indicate that RFB during exercise can result in arterial hypoxemia if RFB is performed with breath-holding at FRC, this mechanism being closely related to the mechanical responses due to lung volume restriction.     

Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses

Recently, it was reported that acute hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s^–1 on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg (P<0.0001) at 30 s of maximal exertion, but further significant changes did not occur as exercise duration increased to 120 s [arterial oxygen tension 72.4 (2) mmHg]. A significant arterial hypoxemia also developed in galloping horses in the acute hypervolemia study [arterial oxygen tension at 30 and 120 s was 76.7 (1.7) and 71.9 (1.6) mmHg, respectively], but significant differences between treatments could not be demonstrated. In both treatments, a similar desaturation of arterial hemoglobin was also observed at 30 s of maximal exercise, which intensified with increasing exercise duration as hyperthermia, acidosis and hypercapnia intensified. Thus, acute expansion of plasma volume did not benefit arterial oxygenation in maximally exercising thoroughbred horses.     

慢性阻塞性肺病日间PaO2、PaCO2与睡眠时血氧的相关研究

目的 探讨慢性阻塞性肺病（ｃｈｒｏｎｉｃ ｏｂｓｔｒｕｃｔｉｖｅ ｐｕｌｍｏｎａｒｙ ｄｉｓｅａｓｅ,ＣＯＰＤ）日间动脉血氧分压（ＰａＯ２）、动脉血二氧化碳分压（ＰａＣＯ２）对夜间血氧的影响。方法 监测３０例ＣＯＰＤ患者和１０例正常对照的夜间血氧水平,按ＰａＯ２、ＰａＣｏ２分组比较。结果 （１）ＰａＯ２〉８ｋＰａ时,睡眠时平均动脉血氧饱和度（ＭＳａＯ２）与日间动脉血氧饱和度（ＳａＯ２）,一秒率（Ｆ     

Intermittent atrial level right-to-left shunt with temporary hypoxemia in a patient during support with a left ventricular assist device

We report a 56-year-old male patient developing hypoxemia after surgical replacement of infected valves of a left ventricular assist device (LVAD, Novacor) which had supported him during the previous 15 months. Contrast transesophageal echocardiography (TEE) revealed an atrial septal defect with intermittent right-to-left shunt across a patent foramen ovale. We postulate that the shunt detected in this patient occurred as a consequence of reduced pulmonary vascular compliance due to positive end-expiratory pressure (PEEP) and an increase of mean intrathoracic pressure. Furthermore, we hypothesize that synchronized LVAD operation exacerbates any potential right-to-left shunt due to the profound left ventricular unloading which occurs during LVAD support. In this first report of a right-to-left shunt from a previously unrecognized patent foramen ovale in a Novacor patient, the subsequent transient hypoxemia could be managed by avoiding PEEP of more than 3 mmHg, and mean airway pressure of more than 11 mmHg and by careful volume replacement in order to prevent the pump from completely emptying the left ventricle (LV) and the left atrium (LA). Thus, prior to every LVAD implantation a transesophageal contrast echocardiography with Valsalva maneuver should be performed to identify intracardiac right-to-left shunt.     

心脏手术后低氧血症

心脏手术后常常发生低氧血症，但常常不引起外科医牛的重视。有些低氧血疗是一过性，对机体不会造成严重影响。但有些低氧血症会明显延长心脏手术后ICU日及平均住院日，增加死亡率。常见原因有心源性、肺源性（包括原有肺的疚病或无肺的基础疾病）。本文就无肺的基础疾病的心脏手术后产生低氧血症的一些情况进行阐述。肺不张、急性肺损伤、心脏手术后隔肌麻痹、手术方式等都是引起心脏手术后低氧血症的常见原因。心脏手术后隔肌麻痹不易诊断。本文就此问题叙述了几种常用方法的利和弊。研究认为在手术早期给予恰当的呼吸末正压及肺活量充气策略可以改善氧合状态。