P0.1 is a useful parameter in setting the level of pressure support ventilation

Objective The purpose of this study was to investigate whether changes in breathing pattern, neuromuscular drive (P0.1), and the work involved in breathing might help to set the individual appropriate level of pressure support ventilation (PSV) in patients with acute respiratory failure (ARF) requiring ventilatory assistance.Design: A prospective, interventional study.Setting An 8-bed multidisciplinary intensive care unit (ICU).Patients Ten patients with ARF due to adult respiratory distress syndrome (ARDS), sepsis or airway infection were included in the study. Chronic obstructive pulmonary disease (COPD) patients with acute exacerbation were excluded. None of these patients was in the weaning process.Interventions We found a level of pressure support able to generate a condition of near-relaxation in each patient, as evidenced by work of breathing (WOB) values close to 0 J/l. This level was called PS 100 and baseline physiological measurements, namely, breathing pattern, P 0.1 and WOB were obtained. Pressure support was then reduced to 85%, 70% and 50% of the initial value and the same set of measurements was obtained.Measurements and results Flow ( ) was measured by a flow sensor (Varflex) positioned between the Y-piece of the breathing circuit and the endotracheal tube. Tidal volume was obtained by numerical integration of the flow signal. Airway pressure (P_aw) was sampled through a catheter attached to the flow sensor. Esophageal pressure (P_es) was measured with a nasogastric tube incorporating an esophageal balloon. The esophageal balloon and flow and pressure sensors were connected to a portable monitor (CP 100 Bicore) that provided realtime display of flow, volume, P_aw and P_es tracings and loops of P_es/V, P_aw/V and /V relationships. The breathing pattern was analyzed from the flow signal. Patient work of breathing (WOB) was calculated by integration of the area of the P_es/V loop. Respiratory drive (P 0.1) was measured at the esophageal pressure change during the first 100 ms of a breath, by the quasiocclusion technique. When pressure support was reduced, we found that the respiration rate significantly increased from PS 100 to PS85, but varied negligibly with lower pressure support levels. Tidal volume behaved in a similar way, decreasing significantly from PS 100 to PS85, but hardly changing at PS 70 and PS 50. In contrast, WOB and P 0.1 increased progressively with decreasing pressure support levels. The changes in WOB were significant at each stage in the trial, whereas P 0.1 increased significantly from PS 100 at other stages. Linear regression analysis revealed a highly positive, significant correlation between WOB and P 0.1 at decreasing PSV levels (r=0.87), whereas the correlation between WOB and ventilatory frequency was less significant (r=0.53). No other correlation was found.Conclusions During pressure support ventilation, P 0.1 may be a more sensitive parameter than the assessment of breathing pattern in setting the optimal level of pressure support in individual patients. Although P 0.1 was measured with an esophageal balloon in the present study, non-invasive techniques can also be used.     

Periventricular- intraventricular hemorrhage in the premature infant- A historical perspective

The objective of this chapter is to trace the evolution of intraventricular hemorrhage in the premature infant highlighting the importance of the germinal matrix, a critical role for cerebral blood flow changes in the genesis of hemorrhage, clinical factors that increase the bleeding risk, and potential preventative strategies. In 1976, neuropathological studies demonstrated capillary rupture within the germinal matrix as the precursor of hemorrhage. In 1980, introduction of cranial ultrasound facilitated diagnosis of intraventricular hemorrhage. In 1979, loss of cerebral autoregulation in sick newborn infants was demonstrated. In the 1980’s, studies demonstrated the importance of intravascular factors in provoking hemorrhage. In 1983, the association of cerebral blood flow velocity fluctuations and subsequent hemorrhage was demonstrated. In 1994, antenatal steroids use to accelerate lung development was recommended. This was associated with an unanticipated reduction in hemorrhage. In the mid 1990’s early indomethacin administration was associated with a reduction of severe hemorrhage.     

经皮球囊二尖瓣成形术10年临床经验

目的：旨在研究本院４００ 例经皮球囊二尖瓣成形术１０ 年的临床经验。　方法：采用改良的Ｉｎｏｕｅ 方法。　结果：经皮球囊二尖瓣成形术即刻成功率９８．３％ （３４４／３５０）,术后二尖瓣面积明显增加,达（１．１１±０．２９）～（２．１９±０．４０）ｃｍ ２。１０５ 例随访９个月～８ 年６ 个月,二尖瓣再狭窄率为１１．４％ （１２／１０５）,死亡率为２．９％ （３／１０５）,二尖瓣置换术为３．８％ （４／１０５）。　结论：经皮球囊二尖瓣成形术近、远期疗效均很好     

44例脓胸的外科治疗

目的：探讨脓胸的治疗方法。方法：根据已出院的44例脓胸患者的治疗资料进行分析。结果：胸腔闭式引流、胸腔灌洗是治疗中不可缺少的手段。结论：在全身治疗的基础上,配合胸腔闭式引流、胸腔灌洗、必要的外科手术可望取得较为理想的治疗结果。     

强直性脊柱炎患者的食管运动功能

研究诱导型一氧化氮合酶 （ｉｎｄｕｃｉｂｌｅ ｎｉｔｒｉｃ 　ｏｘｉｄｅ ｓｙｎｔｈａｓｅ, ｉＮＯＳ）在电离辐射导致的神经细胞凋亡中的作用。 方法：以单剂量２．０ Ｇｙ γ射线照射出生后 ０ ｄ的 Ｗｉｓｔａｒ大鼠,用 ＡＢＣ法检测照射后第 ０．５、１、２、４、６、８、１２、２４、４８小时大脑皮质内ｉＮＯＳ的表达。结果：照射组各时间点均有不同程度的ｉＮＯＳ表达,第６小时达峰值。各对照组未见ｉＮＯＳ表达。结论：ｉＮＯＳ所具有的神经毒作用可能是电离辐射导致的发育中脑神经细胞凋亡的重要因素。     

Inspiratory pressure/maximal inspiratory pressure: does it predict successful extubation in critically ill infants and children?

Objective To evaluate the accuracy of the initial negative inspiratory pressure (PI) to maximal negative inspiratory pressure (PI_max) ratio in predicting extubation outcome for intubated infants and children.Design A prospective study. Setting: Pediatric intensive care unit.Patients A sample of 50 stable intubated pediatric patients who were judged clinically ready for extubation.Methods Using a one-way valve,PI andPI_max were measured in all patients, after which the ratioPI/PI_max was calculated and its accuracy in predicting extubation outcome evaluated.Measurements and results A total of 39 patients (78%) were successfully extubated and 11 patients (22%) were not. The meanPI/PI_max ratio was not significantly different between extubation successes (0.36±0.14) and failures (0.45±0.1) (P>0.05). The cut-off value of 0.3 forPI/PI_max identified in adult patients did not discriminate between extubation success and failure in children. Furthermore, a discriminatory cut-off value other than 0.3 could not be identified for infants and children.Conclusion ThePI/PI_max ratio cannot be used to predict extubation outcome in pediatric patients. Indices that predict extubation outcome in adults should not be extrapolated to infants and children before testing and validation.     

Polyclonal 111In-IgG, 125I-LDL and 125I-endothelin-1 accumulation in experimental arterial wall injury

To test iodine-125 labelled low-density lipoprotein (¹²⁵I-LDL), polyclonal indium-111 labelled immunoglobulin G (¹¹¹In-IgG) and iodine-125 labelled endothelin-1 uptake in metabolically active atheromatous plaques after arterial wall injury, we performed balloon de-endothelialization of carotid arteries or abdominal aortas in 24 New Zealand male rabbits which were fed with a normal diet (n=14) or a hypercholesterolaemic diet (n=10) after surgery. Six weeks later the animals were injected with 200 Ci of (¹²⁵I-LDL), and/or with 100 Ci of ¹¹¹In-IgG or with 9 Ci of ¹²⁵I-endothelin-1. Forty-eight hours later the animals were sacrificed. Carotid arteries and aortas were removed, counted and fixed for autoradiography and light microscopy examination. Contralateral carotid arteries and thoracic aortas served as controls.Significant ¹¹¹In-IgG uptake was observed in the injured arteries at autoradiography, with localization mainly in the healing edges, and at well counting. The percentage of the injected dose per gram (%D.inj/g) was 0.0188±0.06 versus 0.0059±0.003 in controls (P< 0.05). There was no difference in ¹¹¹In-IgG uptake between arteries with injury alone and those with active atheroma formation at the site of the injury. Significant (¹²⁵I-LDL), uptake was observed only when lipid deposition was present at light microscopy (%D.inj/g of 0.0024±0.0005 vs 0.0010±0.0003 in controls, P < 0.05). ¹²⁵I-endothelin-1 accumulation was observed in four of five injured aortas both at autoradiography, with diffuse localization, and at well counting (%D.inj/g of 0.0012±0.0004 in the abdominal aortas vs 0.0008±0.0003 in the thoracic aortas).Polyclonal IgG may accumulate in injured arteries without active atheroma formation. Inflammatory reaction at the site of the injury may cause ¹¹¹In-IgG uptake independently of atheromatous plaque formation. LDL accumulation takes place only with active atheroma formation at the site of the injury. Use of labelled peptides such as endothelin-1 may provide further insight into the mechanisms of atheromatous plaque formation.     

Electron microscopy and X-ray microanalyses of uterine epithelium from lead-injected mice in an experimental delay of implantation

Mice in experimental delay of implantation were injected intravenously with 75 g · g^–1 body weight of lead chloride, corresponding to a dose of lead of about 56 g · g^–1 body weight. Delay of implantation was obtained by ovariectomy 3 days after mating followed by a depot dose of progesterone every fifth day. Electron microscopy showed that the uterine lumen, which was closed in control mice, was opened in lead-injected mice. This morphology suggested that lead caused an increase in uterine secretion. X-ray microanalysis of pyroantimonate precipitates in the uterine epithelium of injected mice demonstrated lead in the precipitates, suggesting that lead could have a direct effect on the function of the uterine epithelium and that lead also could be secreted into the uterine lumen and affect the blastocysts.     

Combined negative inotropic effects of calcium entry blockers and isoflurane on canine isolated heart muscles

The combined negative inotropic effects of isoflurane and calcium entry blockers (verapamil, diltiazem, nifedipine, nicardipine) were studied utilizing isolated heart preparations of ventricular muscles from dogs. All of these calcium entry blockers exerted dose-dependent decreases in maximal velocity of shortening (Vmax), maximal developed isometric force (Fm), and the maximal first derivative of Fm (maximal dF/dt). Dose-dependent decreases of these variables of muscle mechanics were augmented in isoflurane-depressed myocardium. At equimolar concentrations, direct myocardial depression was demonstrated in the following order of severity: nifedipine > diltiazem = verapamil > nicardipine. Percent depressions of Vmax, Fm and maximal dF/dt were significantly greater in muscles when calcium entry blockers were combined with 1MAC isoflurane than in muscles of calcium entry blockers alone. These data suggest that the negative inotropic effects of verapamil, diltiazem, nifedipine, and nicardipine were potentiated by isoflurane.(Nakata F, Kemmotsu O: Combined negative inotropic effects of calcium entry blockers and isoflurane on canine isolated heart muscles. J Anesth 5: 48–55, 1991)     

Hereditary neuropathy with liability to pressure palsies

Summary Clinical, neurophysiological and pathological investigations were carried out in 11 affected members of 2 families with hereditary neuropathy with liability to pressure palsies (HNPP). The observations were related to findings in 261 cases of 47 families published in the literature. It was concluded that HNPP is a nosological entity characterized by the following diagnostic criteria: (1) an autosomal dominant inheritance; (2) the clinical presentation of a recurrent mononeuropathy simplex or multiplex, frequently related to an inadequate trauma to peripheral nerves; (3) a significant slowing of motor and sensory conduction velocity in clinically affected, but also in clinically unaffected nerves; (4) characteristic morphological findings in sural nerve biopsy featuring tomaculous swellings of myelin sheaths, transnodal myelination and segmental demyelination. The pathogenesis of HNPP is not clear. Hypothetical explanations of the pathogenesis of HNPP are discussed.In memory of Albert Bischoff (1921–1981), Professor of Neurology, University of Berne