A tidal ventilation model for oxygenation in respiratory failure

We develop tidal-ventilation pulmonary gas-exchange equations that allow pulmonary shunt to have different values during expiration and inspiration, in accordance with lung collapse and recruitment during lung dysfunction (Am. J. Respir. Crit. Care Med. 158 (1998) 1636). Their solutions are tested against published animal data from intravascular oxygen tension and saturation sensors. These equations provide one explanation for (i) observed physiological phenomena, such as within-breath fluctuations in arterial oxygen saturation and blood-gas tension; and (ii) conventional (time averaged) blood-gas sample oxygen tensions. We suggest that tidal-ventilation models are needed to describe within-breath fluctuations in arterial oxygen saturation and blood-gas tension in acute respiratory distress syndrome (ARDS) subjects. Both the amplitude of these oxygen saturation and tension fluctuations, and the mean oxygen blood-gas values, are affected by physiological variables such as inspired oxygen concentration, lung volume, and the inspiratory:expiratory (I:E) ratio, as well as by changes in pulmonary shunt during the respiratory cycle.     

Evidence for central reorganization of ventilatory chemoreflex pathways in the cat during regeneration of visceral afferents in the carotid sinus nerve

There are two sets of peripheral arterial chemoreceptors in the cat, the carotid bodies innervated by the carotid sinus nerve and the aortic bodies with afferents in the aortic depressor nerves. Reflex stimulation of ventilation in response to hypoxia is abolished acutely after interrupting the sensory pathway from the carotid body chemoreceptors in the cat even though the reflex pathway from the aortic body chemoreceptors is intact. However, in chronically maintained preparations, there is a restoration of the hypoxic response which is mediated by the aortic chemoreflex pathway. It was proposed that restoration was due to a ‘central reorganization’ of chemoreflex pathways which followed interruption of the sensory pathway from the carotid bodies and that the reorganization enhanced the efficacy of the aortic ventilation chemoreflex. This proposal was tested in the present experiments by measuring reflex ventilatory and cardiovascular responses to electrical stimulation of the sensory nerves containing aortic and carotid chemoreceptor afferents following bilateral interruption of carotid sinus nerves and carotid body resection. Responses measured acutely (1–6 h) after interruption were compared with those measured 60–80 and 110–140 days later. At 60–80 days, a chemoreflex response (increase in tidal volume of ventilation) to stimulation of the interrupted carotid sinus sensory pathway was markedly attenuated while the response to stimulation of the uninterrupted pathway in aortic depressor nerves was enhanced. At 110–140 days, the tidal volume response to carotid sinus nerve stimulation was greatly enhanced while the aortic depressor nerve response declined from the elevated level. There were significant but less pronounced changes in the response of other ventilatory and cardiovascular variables to aortic depressor nerve and carotid sinus nerve stimulation.The results support the idea that there is a ‘central reorganization’ of chemoreflex pathways which is reflected functionally by changes in the efficacy of reflexes evoked from aortic depressor nerve and carotid sinus nerve. The changes are analagous to those occurring in somatic reflexes during regeneration of sensory nerves. It is suggested that the changes in efficacy of carotid sinus nerve reflexes are due to a degenerative loss of synapses of the central projections of interrupted carotid sinus nerve sensory axons (degenerative atrophy) and subsequent regenerative like changes (regenerative proliferation) in the central projections. The changes in the efficacy of aortic depressor nerve reflexes may be attributed to formation of new synapses by converging central projections of this uninterrupted pathway (reactive synaptogenesis) and subsequent regression of the newly formed synapses.     

小潮气量通气在急性呼吸窘迫综合征中的应用

应用小潮气量通气致容许性高碳酸血症方法对11例急性呼吸窘迫综合征（ARDS）进行临床观察。设定潮气量为6．4±1．1ml／kg,保持动脉血二氧化碳（PaCQ2）为5．97±1．41kPa,血氧分压8．54±3．19kPa。结果7例存活,未发现气压伤。说明小潮气量通气致一定程度高碳酸血症是临床上值得推荐使用的方法。     

支气管舒张试验在0～6岁儿童喘息性疾病中的应用

目的利用潮气呼吸法进行儿童的支气管舒张试验,探讨其在0～6岁儿童喘息性疾病中的应用价值。方法2006年4～11月就诊于安徽医科大学附属省立医院儿科门诊及住院的儿童喘息性疾病244例,以沙丁胺醇作为支气管舒张药物,用潮气呼吸法分析评价小年龄喘息性疾病儿童吸入药物前后肺功能的变化,以探讨支气管舒张试验在该年龄段的应用价值。结果(1)吸入支气管舒张剂前后,以达峰时间比(TPTEF/TE)和达峰容积比(VPEF/VE)任意一个改善率≥15%为阳性标准,肺功能异常组阳性率明显高于正常组。(2)吸入支气管舒张药物,肺功能差值为负值率正常组明显高于异常组。(3)肺功能异常组各年龄段间支气管舒张试验阳性率无明显差异。结论支气管舒张试验在肺功能异常时应用较正常时更有价值。     

全麻期间呼气末和动脉血二氧化碳分压的变化及其影响因素

本文对比观察21例神经外科病人50～60% N_2O-O_2-安(异)氟醚麻醉期间呼气末二氧化碳分压(P_(ET)CO_2)和动脉血二氧化碳分压(PaCO_2)的变化。结果表明麻醉前自主呼吸时或术毕自主呼吸恢复后 PaCO2 和 P_(ET)CO_2 的相关性明显高于麻醉期间间歇正压通气时,潮气量对Pa_(-ET)CO_2 有一定的影响。结论:自主呼吸时 P_(ET)CO_2 能较正确地反映 PaCO_2;全麻控制呼吸期间以 P_(ET)CO_2 估测 PaCO_2 的准确性下降;采用 P_(ET)CO_2 和潮气量多元估测 PaCO_2 可提高准确度。     

小潮气量结合低水平呼气末气道正压在软镜肾脏碎石中的应用

目的:探讨小潮气量结合低水平呼气末气道正压在软镜肾脏碎石中的临床应用价值.方法:选择患者80例,分为两组,各40例,呼吸控制上,观察组采用小潮气量低呼气末正压维持,对照组采用间停呼吸处理,比较两组干预后30min血气分析结果、术毕两组TNF-a、IL-6和CRP水平及两组手术相关指标.结果:干预后30min,观察组pH水平低于对照组(P<0.05),PCO2水平低于对照组(P<0.05),术毕,观察组TNF-a、IL-6和CRP水平均低于对照组(P<0.05),观察组手术时间短于对照组(P<0.05),呼吸影响操作例数及软镜治疗失败比例低于对照组(P<0.05).结论:小潮气量结合低水平呼气末气道正压用于软镜下钬激光肾脏碎石,维持患者血气分析结果正常,显著降低手术、麻醉应激对患者影响,更利于手术操作.     

低潮气量机械通气对慢性肺病患者全麻术中肺呼吸的保护作用

目的：观察低潮气量加低水平呼气末正压通气在慢性肺部疾病患者全麻手术中对肺呼吸功能的影响。方法：将慢性肺部疾病拟行非肺部手术患者100例,随机分为保护性通气组和常规通气组,每组各50例。保护性通气组（A组）,通气模式采用低潮气量加低水平呼气末正压（PEEP）机械通气;常规通气组（B组）,采用常规方法通气。分别于麻醉诱导前（T0）、机械通气1h（T1）、拔管后15min（T2）、术后6h（T3）采动脉血行血气分析,并记录各时点的动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）、气道峰压（Ppeak）、气道平台压（Pplat）、平均动脉压（MAP）。结果：T1、T2、T3时A组PaO2水平高于B组,T1时A组Ppeak、eplat低于B组,差异有统计学意义（P〈0．05）;两组各时点PaCO2、MAP比较,差异无统计学意义（P〉0．05）。结论：慢性肺部疾病患者全麻手术中,低潮气量加低水平呼气末正压通气的肺保护性通气策略对肺的呼吸功能有保护作用。     

保护性通气策略在老年髋关节手术全身麻醉期间的应用

目的探讨保护性通气策略应用于老年髋关节手术全身麻醉期间的临床有效性。方法选择择期老年全身麻醉下髋关节手术患者40例,随机分为:常规机械通气组(C组,20例):潮气量(Vt)=9 m L/kg理想体重(IBW),初始呼吸频率(f)=12次/min,吸气呼气时间比(I∶E)=1∶2;保护性肺通气组(P组,20例):Vt=7 m L/kg IBW,初始呼吸频率(f)=12次/min,I∶E=1∶2,呼气末正压设为6 cm H2O,每30分钟手法肺复张1次。术中吸入氧气浓度40%,调整呼吸频率维持PETCO235~45 mm Hg。分别于麻醉诱导前(T1)、气管插管后5 min(T2)、机械通气1.5 h(T3)、拔除气管导管后1 h(T4)、术后3 d(T5)观察记录HR、MAP、气道峰压(Ppeak)、气道平台压(Pmean),计算肺动态顺应性(Cdyn);血气分析仪测定Pa O2、Pa CO2和Hb;观察术后肺部并发症。结果C组术后拔除气管导管后1 h和术后3 d,Pa O2和氧合指数(Pa O2/Fi O2)均较术前降低(P<0.05),P组Pa O2和氧合指数在拔除气管导管后1 h较术前降低(P<0.05),但术后3 d无明显差异,且在机械通气1.5 h、拔除气管导管后1 h和术后3 d均较C组显著增高(P<0.05)。P组在机械通气期间Ppeak和Pmean均高于C组(P<0.05)。两组在机械通气1.5 h后Cdyn降低(P<0.05),但P组高于C组(P<0.05)。P组术后肺部并发症发生率明显低于C组(P<0.05)。结论肺保护策略能够有效提高老年髋关节手术患者肺顺应性,改善氧合,减少肺部并发症,利于呼吸功能恢复。     

Lung function measurements in awake compared to sleeping newborn infants.

Tidal breathing flow-volume loops were recorded in 19 healthy newborn infants when awake and asleep. This preceded and followed measurements of passive lung mechanics (by single breath occlusion). Our aim was to evaluate possible differences in lung function due to state of arousal or any influence of the occlusion technique. Expiratory volumes and flow rates were larger in awake than in sleeping infants before, but not after occlusion measurements. In sleeping, but not in awake infants, expiratory volumes and flow rates were higher after occlusion than before. Respiratory system compliance was significantly larger in sleeping than awake infants, while differences in respiratory system resistance and airway plateau pressure did not reach a significant level. Our results show that lung function can be measured in awake as well as sleeping infants, but differs significantly according to their arousal state, and whether tidal expiratory flow measurements are performed before or after airway occlusion measurements. Separate reference values for awake and sleeping infants may, therefore, be required. Marked intrasubject variability was found in the occlusion measurements, and criteria for acceptable measurements need to be defined.