胸内正压对正常人左室功能的直接影响及其力学原理
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摘要
胸内压力变化对血流动力学有明确影响，但其机制至今不清。一百三十多年来，国内外众多学者从不同角度广泛研究了该现象的机制，先后提出十多种假说，大多数假说都被后来的研究推翻。目前，占优势的主要有三种假说：肺容量增加学说、左右心室充盈相互竞争学说和心包添压学说，但都存在问题。学术界普遍认为真正的机理仍不清楚。
我们研究发现，以上假说之所以未能成功解释这一现象是因为以往研究或理论只涉及到心功能及血流动力学的改变与由其引起的心脏功能改变而忽视了胸内压的直接力学作用对心脏收缩与舒张功能的影响。因此，我们设计了这一课题，利用乏氏动作模拟并放大平静呼吸呼气相胸内压增高时的情况，观测乏氏动作张力期正常人左室功能变化，探讨胸内正压的直接力学作用对正常人左室功能的影响及其机制。
第一部分：正常人乏氏动作张力期左室充盈变化及其力学机制
目的
应用超声心动图探讨正常人乏氏动作张力期左室充盈变化及其力学机制。
方法
1、实验对象
30名健康志愿者，男性21名，女性9名，平均年龄40.1岁（23-66岁）。既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的胸内压测定装置。使用表式血压计改装而成，将表式血压计袖带的一部分取下，接上一口鼻面罩(可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致)。口鼻面罩的一个末端与压力表式指针相连，另一末端与压力传感器相连，后者通过导线可连接于超声诊断仪脉冲通道，使胸内压曲线同步显示于荧光屏。
2.2西门子Sequoia512与西门子S2000超声诊断仪，4V1c探头，频率2.5～4.0MHz。
3、方法
左后侧倾斜卧位，连接同步心电图。超声心动图观测30例健康志愿者在初始时、乏氏动作张力期第1个心动周期及第2个心动周期时左室充盈指标（E、A、E/A、e及E/e）的变化。实时超声检查中存储受试者乏氏动作张力期超声图像。分析初始时、乏氏动作张力期第1个心动周期、第2个心动周期时左室流入道血流速度（E峰，A峰）及二尖瓣环舒张早期运动速度（e），计算左室舒张功能（E/A值）及左室舒张早期充盈压（E/e）的变化。结果
与初始时比较，第1个心动周期时E、E/A及E/e增大（P＜0.05）；与第1个心动周期比较，第2个心动周期时E、E/A及E/e减低（P＜0.05）。结论
正常人乏氏动作张力期第2个心动周期时左室充盈即减低，这与以往认为张力期4-5个心动周期后左室充盈开始减低不同。胸内正压降低左心系统与回流肺静脉跨壁压力，增加血流阻力可能是其原因。
第二部分：曲率半径法评价正常人乏氏动作张力期室间隔运动
目的
使用曲率半径法评价正常人标准乏氏动作张力期室间隔形变与运动。
方法
1、实验对象
23例健康志愿者，男性15名，女性8名，平均年龄32.6岁（23-49岁）。入选条件：既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的胸内压力测定装置。使用表式血压计改装而成，将表式血压计袖带的一部分取下，接上一口鼻面罩(可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致)。口鼻面罩的一个末端与压力表式指针相连，另一末端与压力传感器相连。
2.2西门子Sequoia512与西门子S2000超声诊断仪，4V1c探头，频率2.5～4.0MHz。
3、方法
所有测试均在晚上进行，至少晚饭后2小时。先瞩受试者平静呼吸，左后侧倾斜卧位，连接同步心电图，行常规超声心动图检查。胸骨旁左室短轴二尖瓣腱索水平分别获取平静吸气相与呼气相的二维图像。然后瞩受试者捂紧胸压测定装置的口鼻面罩做乏氏动作，要求呼气压在0.5秒之内达到40mmHg，在实时超声检查中存储受试者标准乏氏动作张力期5s及10s的二维图像。使用自制的曲率半径测量软件计算平静吸气相、呼气相、乏氏动作张力期5s及10s时室间隔形变的曲率半径。
结果
室间隔曲率半径吸气相＞乏氏动作张力期10s＞呼气相＞乏氏动作张力期5s；两两之间比较，差异均有显著意义（P＜0.01）。
结论
正常人乏氏动作张力期5s时室间隔仍向右室侧移位，10s时室间隔形变介于吸气相与呼气相之间，无明显摆动。
第三部分：胸内正压对正常人左室充盈的直接影响及其力学机制
目的
应用超声心动图观测胸内正压对正常人左室充盈的直接影响并探讨其力学机制。
方法
1、实验对象
30名健康志愿者，男性21名，女性9名，平均年龄40.1岁（23-66岁）。入选条件：既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的胸内压测定装置。使用表式血压计改装而成，将表式血压计袖带的一部分取下，接上一口鼻面罩(可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致)。口鼻面罩的一个末端与压力表式指针相连，另一末端与压力传感器相连，后者通过导线可连接于西门子Sequoia512超声诊断仪的脉冲通道。
2.2西门子Sequoia512与西门子S2000超声诊断仪，4V1c探头，频率2.5～4.0MHz。
3、超声检查
所有测试均在晚上进行，至少晚饭后2小时。先瞩受试者平静呼吸，左后侧倾斜卧位，抬高左臂至枕后以伸展肋骨增大超声波透声窗，连接同步心电图，行常规超声心动图检查。观察心率呈稳定状态3分钟后储存心尖四腔观二尖瓣口频谱多普勒超声及二尖瓣环组织多普勒超声图像作为初始时的实验资料。然后瞩受试者捂紧气压测定装置的口鼻面罩做乏氏动作，要求呼气压在0.5秒之内达到40mmHg，在实时超声检查中存储受试者乏氏动作张力期超声图像。分析初始时与标准乏氏动作张力期10s时左室流入道血流速度（E峰、A峰）、E/A值、二尖瓣环舒张早期运动速度(e)及舒张早期充盈压（E/e）的变化。
4、统计学分析采用SPSS13.0统计软件，计量资料以均数±标准差（±s）
表示。两组资料比较用配对的t检验。P＜0.05为有统计学意义。结果
与初始时比较，标准乏氏动作张力期10秒时经二尖瓣血流速度E峰减低（P＜0.05），A峰没有变化（P＞0.05），E/A值减低（P＜0.05）；e没有变化（P＞0.05），E/e值减低（P＜0.05）。
结论
1，胸内正压对左室游离壁的力学作用阻碍了左室的舒张运动，引起E峰及E/A值减低；2，胸内正压降低了肺静脉系统与心脏的跨壁压力，增加了血流阻力也是导致肺静脉系统与左室血液回流减少，E峰减低，E/e值减低的一个原因。
第四部分：胸内正压对正常人左室收缩功能的直接影响及其力学机制
目的
应用超声心动图观测胸内正压对正常人左室收缩功能的直接影响并探讨其力学机制。
方法
1、实验对象
20名健康志愿者，男性15名，女性5名，平均年龄38.3岁（24-62岁）。入选条件：既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的乏氏动作负荷压定量装置。使用表式血压计改装而成，将原表式血压计袖带的一部分取下，接上一口鼻面罩，可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致。口鼻面罩的一个末端与压力表式指针相连，可定量与监测乏氏动作负荷压力。
2.2GE Vivid7彩色多普勒超声诊断仪，M3S探头，探头频率1.0～3.0MHz。
3、超声检查
所有测试均在晚上进行，至少晚饭后2小时。先瞩受试者平静呼吸，左后侧倾斜卧位，抬高左臂至枕后以伸展肋骨增大超声波透声窗，连接同步心电图，行常规超声心动图检查。观察心率呈稳定状态3分钟后记录并储存心尖四腔观或胸旁四腔观的二维超声及脉冲多普勒超声图像作为初始时的实验资料。然后瞩受试者捂紧气压测定装置的口鼻面罩做乏氏动作，要求呼气压在0.5秒之内达到40mmHg，在实时超声检查中存储受试者乏氏动作张力期心尖四腔观或胸旁四腔观的二维及脉冲多普勒超声图像。分析初始时与标准乏氏动作张力期10s时左室舒张末容积（LVEDV）、左室收缩末容积(LVESV)、每搏量(SV)、射血分值（EF）、心率（HR）、心输出量（CO）、主动脉最大血流速度（PV）及平均血流加速度（MAC）的变化。
4、统计学分析采用SPSS13.0统计软件，计量资料以均数±标准差（±s）
表示。两组资料比较用配对的t检验。P＜0.05为有统计学意义。
结果
与初始时比较，标准乏氏动作张力期10秒时LVEDV、LVESV及SV减低而HR增快（P均＜0.001），EF值增加，但无统计学意义（P＞0.05），CO及PV减低（P＜0.05），MAC没有变化，（P＞0.05）。
结论
胸内正压对左室游离壁的力学作用参与左室的收缩运动，其方向与左室本身的收缩力方向基本一致，两者合力增大，促进了左室的收缩运动，会引起EF值增加；胸内正常增加了血流阻力，引起回流量减低，导致SV、CO及PV减低。
Intrathoracic pressure changes with respiration, which exerts mechanicaleffects on cardiovascular hemodynamics. However, the mechanism of thisphenomenon still remains obscure. For over one hundred and thirty years, themechanism study for this phenomenon has challenged investigators and manyproposed hypotheses were proved to be irrational. Some have suggested thatinspiration increases venous capacitance of the pulmonary vessels, therebyreducing venous return to the left heart. But the results of the study by Scharf SMverified that without expansion of the pulmonary vessels, left heart output willstill decrease. Some have proposed that LV filling during inspiration decreasesbecause of compression of the LV from the enlarging right ventricle, however,this is just the description of the phenomenon but not the mechanism. It is alsoproposed that LV ejection is impeded by the fall of the intrathoracic pressurearound the heart comparable to an increase in arterial pressure, however, whichseems the consequence of decreased intrathoracic pressure and can notreasonably explain it.
We find that the above hypotheses failing to explain this phenomenon is that previous studies only involved the changes of LV hemodynamics and theresulting changes in LV function while neglected the directly mechanical effectsof intrathoracic pressure on LV ejection and filling. Accordingly, using theValsalva maneuver (VM) to simulate and amplify the situation of expiratoryphase, we designed these studies with echocardiography to evaluate the changesof LV ejection and filling induced directly by increased positive intrathoracicpressure.
Part1. Changes of left ventricular filling during the strain phase of Valsalvamaneuver in healthy subjects and its mechanism
Objective
The aim of this study was to explore changes of left ventricular filling duringthe strain phase of Valsalva maneuver (VM) and its mechanism.
Methods
30healthy volunteers were recruited to perform VM with a load of40mmHg.Left ventricular filling parameters (E, A, E/A ratio, e and E/e ratio) weredetermined by echocardiography at baseline, at the first beat and at the secondbeat during the strain phase of VM, respectively.
Results
Compared to those at baseline, E, E/A ratio and E/e ratio increased (P＜0.05）while A and e did not change (P＞0.05）at the first beat during the strain phase;Compared to those at the first beat during the strain phase, E, E/A ratio and E/eratio decreased (P＜0.05）while A and e did not change (P＞0.05）at the secondbeat during the strain phase.
Conclusions
Left ventricular filling decreased at the second beat during the strain phase of VM, which is different from the present knowledge that left ventricular fillingwould begin to decrease4-5beats later during the strain phase of VM. Positiveintrathoracic pressure decreases left-side heart and pulmonary vessel’ transmuralpressure while increases the blood resistance, which might be the reason that E,E/A ratio and E/e ratio decreased at the second beat during the strain phase ofVM.
Part2. Evaluation of the motion of septum during the strain phase ofValsalva maneuver in normal person by radius of curvature
Objective
The aim of this study was to evaluate the displacement of septum during thestrain phase of Valsalva maneuver (VM) in normal person by radius of curvature(RC).
Methods
23healthy volunteers were recruited to perform VM with a load of40mmHglasted for10seconds. The two-dimensional short-axis images of left ventricularduring quiet breath and during the VM were recorded and were analyzed withself-designed software to gain RC of septum and to calculate the changes.
Results
RC of septum during inspiration＞10th second during the VM＞duringexpiration＞5th second during the VM, any two of which, there is a significantchange (P＜0.01）.
Conclusions
During the strain phase of VM, septum will displace towards right ventricular at the5th second while there is no significant displacement at10th second.
Part3. Mechanical Effects of Positive Intrathoracic Pressure on LeftVentricular Filling in Healthy Subjects and Its Mechanism
Objective
Our aim was to explore the mechanical effects of positive intrathoracicpressure on left ventricular (LV) filling in healthy subjects and its mechanism.
Methods
1、 Subjects
We recruited thirty healthy volunteers,21men and9women, with a meanage of39±17years（range,23to66years), height of171±8cm, and weight of68±9kg in this study. None of these subjects had clinical symptoms, signs orhistory of any disease as determined by detailed inquiry, physical examination,electrocardiogram (ECG), chest X-ray and echocardiography. Alcohol, tobacco,strong tea and coffee were not allowed on the day of the test.
2、 Quantification of the load of VM
A self-made device was used to quantify and standardize the load of VM,which was modified from a watch style sphygmomanometer and has beendescribed in our previous study. Differently, a facial mask that could cut offventilation from both mouth and nose was used in the present study. Its functioncan compare with the previously used. All subjects were trained on how to usethe device to quantify and standardize a VM
3、 Examining protocol
At first, the subjects were asked to breathe quietly and naturally. After the subjects’ heart rate remaining at a stable level, echocardiography images wererecorded. Then the subjects were instructed to perform VM, at a load of40mmHg lasted for10seconds, with the self-made device quantified and standardized.Echocardiography images were recorded during the strain phase of VM.Measurements were performed at rest and at10th second during the strain phase.During measurements, investigators were blinded to the subjects’ data. HR wasobtained from the simultaneously recorded ECG. LV inflow velocities weredetermined using pulse-wave Doppler. Early diastolic flow velocity (E) and latediastolic flow velocity（A) were analyzed and E/A ratio was calculated. Earlydiastolic velocity (e) of the septal portion of the mitral annulus was determinedusing pulse-wave tissue Doppler imaging and E/e ratio was calculated.
4、 Statistics analysis
SPSS13.0statistic software was used. Data were expressed as mean±standard deviation. Continuous data were compared with paired Student’s t-testwhen appropriate. Probability ratio P＜0.05was considered statisticallysignificant.
Results
Compared to the rest, at10th second, early diastolic velocity (E)significantly decreased (P＜0.05), late diastolic velocity (A) insignificantlydecreased (P＞0.05) and E/A ratio significantly decreased (P＜0.05); earlydiastolic velocity (e) of the mitral annulus did not changed (P＞0.05) and E/eratio significantly decreased (P＜0.05), heart rate (HR) dramatically increased (P＜0.001).
Conclusions
Mechanical effect of positive intrathoracic pressure on LV free wall impedesLV diastolic motion, which could cause the decrease of E and E/A ratio. Positive intrathoracic pressure increases the flow resistance of LV and pulmonaryvasculature, which may contribute to the decrease of E and E/e ratio.
Part4. Mechanical Effects of Positive Intrathoracic Pressure on LeftVentricular systolic function in Healthy Subjects and Its Mechanism
Objective
Our aim was to explore the mechanical effects of positive intrathoracicpressure on left ventricular (LV) systolic function in healthy subjects and itsmechanism.
Methods
1、Subjects
We recruited twenty healthy volunteers,15men and5women, with a meanage of38.3years（range,24to62years). None of these subjects had the signs,symptoms, or history of disease as determined by history-taking, physicalexamination, electrocardiography (ECG), chest radiography, andechocardiography. Consumption of alcohol, tobacco, strong tea or coffee was notallowed on the test day.
2、Quantification of VM
A self-made device which was refitted from a watch-stylesphygmomanometer, as described in our previous study. A face-mask that couldcut off ventilation from the mouth and nose (and whose function could becompared with the face-mask used in our previous study) was employed. Allsubjects were trained on how to use the device to quantify and standardize a VM
2、Examining protocol
All experiments were undertaken in the evening≥2h after a light supper.GE Vivid7(GE Healthcare, Piscataway, NJ, USA) echocardiographic systemswere used with probe frequencies of2.5–4.0MHz.
Subjects were initially asked to breathe quietly and naturally. After a stableHR was achieved, echocardiographic images were recorded. Subjects were theninstructed to carry out the VM at a load of40mmHg for10s. This action wascarefully monitored using a self-made device. Echocardiographic images werealso recorded at10s during the strain phase. Measurements were recorded at restand at10s during the strain phase. During measurements, investigators wereblinded to the subjects’ data. Off-line analyses included left-ventricularend-diastolic volume (LVEDV), left-ventricular end-systolic volume (LVESV),stroke volume (SV), ejection fraction (EF), cardiac output (CO), peak aorticvelocity(PV) and mean local acceleration(MAC). HR was obtained from thesimultaneously recorded ECG.
4、 Statistics analysis
SPSS13.0statistical software (SPSS, Chicago, IL, USA) was used. Data aremean±standard deviation. Continuous data were compared using the pairedStudent’s t-test if appropriate. P＜0.05was considered significant.
Results
Compared to the rest, at10th second, LVEDV, LVESV and LV strokevolume (SV) dramatically decreased (P＜0.001) while heart rate (HR)dramatically increased (P＜0.001), and ejection fraction (EF) insignificantlyincreased (P＞0.05), CO and PV significantly decreased (P＜0.05), MAC hadnot changed (P＞0.05).Conclusions
Mechanical effects of positive intrathoracic pressure acts on LV free wall, itsdirection is nearly identical to that for the direction of the LV contraction force.Hence, cardiac systolic was enhanced and EF increased at10s during the strainphase of the VM. Mechanical effects of positive intrathoracic pressure increasesthe flow resistance of LV and pulmonary vasculature, which may contribute tothe decrease of blood volume, then the decrease of CO and PV.
我们研究发现，以上假说之所以未能成功解释这一现象是因为以往研究或理论只涉及到心功能及血流动力学的改变与由其引起的心脏功能改变而忽视了胸内压的直接力学作用对心脏收缩与舒张功能的影响。因此，我们设计了这一课题，利用乏氏动作模拟并放大平静呼吸呼气相胸内压增高时的情况，观测乏氏动作张力期正常人左室功能变化，探讨胸内正压的直接力学作用对正常人左室功能的影响及其机制。
第一部分：正常人乏氏动作张力期左室充盈变化及其力学机制
目的
应用超声心动图探讨正常人乏氏动作张力期左室充盈变化及其力学机制。
方法
1、实验对象
30名健康志愿者，男性21名，女性9名，平均年龄40.1岁（23-66岁）。既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的胸内压测定装置。使用表式血压计改装而成，将表式血压计袖带的一部分取下，接上一口鼻面罩(可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致)。口鼻面罩的一个末端与压力表式指针相连，另一末端与压力传感器相连，后者通过导线可连接于超声诊断仪脉冲通道，使胸内压曲线同步显示于荧光屏。
2.2西门子Sequoia512与西门子S2000超声诊断仪，4V1c探头，频率2.5～4.0MHz。
3、方法
左后侧倾斜卧位，连接同步心电图。超声心动图观测30例健康志愿者在初始时、乏氏动作张力期第1个心动周期及第2个心动周期时左室充盈指标（E、A、E/A、e及E/e）的变化。实时超声检查中存储受试者乏氏动作张力期超声图像。分析初始时、乏氏动作张力期第1个心动周期、第2个心动周期时左室流入道血流速度（E峰，A峰）及二尖瓣环舒张早期运动速度（e），计算左室舒张功能（E/A值）及左室舒张早期充盈压（E/e）的变化。结果
与初始时比较，第1个心动周期时E、E/A及E/e增大（P＜0.05）；与第1个心动周期比较，第2个心动周期时E、E/A及E/e减低（P＜0.05）。结论
正常人乏氏动作张力期第2个心动周期时左室充盈即减低，这与以往认为张力期4-5个心动周期后左室充盈开始减低不同。胸内正压降低左心系统与回流肺静脉跨壁压力，增加血流阻力可能是其原因。
第二部分：曲率半径法评价正常人乏氏动作张力期室间隔运动
目的
使用曲率半径法评价正常人标准乏氏动作张力期室间隔形变与运动。
方法
1、实验对象
23例健康志愿者，男性15名，女性8名，平均年龄32.6岁（23-49岁）。入选条件：既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的胸内压力测定装置。使用表式血压计改装而成，将表式血压计袖带的一部分取下，接上一口鼻面罩(可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致)。口鼻面罩的一个末端与压力表式指针相连，另一末端与压力传感器相连。
2.2西门子Sequoia512与西门子S2000超声诊断仪，4V1c探头，频率2.5～4.0MHz。
3、方法
所有测试均在晚上进行，至少晚饭后2小时。先瞩受试者平静呼吸，左后侧倾斜卧位，连接同步心电图，行常规超声心动图检查。胸骨旁左室短轴二尖瓣腱索水平分别获取平静吸气相与呼气相的二维图像。然后瞩受试者捂紧胸压测定装置的口鼻面罩做乏氏动作，要求呼气压在0.5秒之内达到40mmHg，在实时超声检查中存储受试者标准乏氏动作张力期5s及10s的二维图像。使用自制的曲率半径测量软件计算平静吸气相、呼气相、乏氏动作张力期5s及10s时室间隔形变的曲率半径。
结果
室间隔曲率半径吸气相＞乏氏动作张力期10s＞呼气相＞乏氏动作张力期5s；两两之间比较，差异均有显著意义（P＜0.01）。
结论
正常人乏氏动作张力期5s时室间隔仍向右室侧移位，10s时室间隔形变介于吸气相与呼气相之间，无明显摆动。
第三部分：胸内正压对正常人左室充盈的直接影响及其力学机制
目的
应用超声心动图观测胸内正压对正常人左室充盈的直接影响并探讨其力学机制。
方法
1、实验对象
30名健康志愿者，男性21名，女性9名，平均年龄40.1岁（23-66岁）。入选条件：既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的胸内压测定装置。使用表式血压计改装而成，将表式血压计袖带的一部分取下，接上一口鼻面罩(可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致)。口鼻面罩的一个末端与压力表式指针相连，另一末端与压力传感器相连，后者通过导线可连接于西门子Sequoia512超声诊断仪的脉冲通道。
2.2西门子Sequoia512与西门子S2000超声诊断仪，4V1c探头，频率2.5～4.0MHz。
3、超声检查
所有测试均在晚上进行，至少晚饭后2小时。先瞩受试者平静呼吸，左后侧倾斜卧位，抬高左臂至枕后以伸展肋骨增大超声波透声窗，连接同步心电图，行常规超声心动图检查。观察心率呈稳定状态3分钟后储存心尖四腔观二尖瓣口频谱多普勒超声及二尖瓣环组织多普勒超声图像作为初始时的实验资料。然后瞩受试者捂紧气压测定装置的口鼻面罩做乏氏动作，要求呼气压在0.5秒之内达到40mmHg，在实时超声检查中存储受试者乏氏动作张力期超声图像。分析初始时与标准乏氏动作张力期10s时左室流入道血流速度（E峰、A峰）、E/A值、二尖瓣环舒张早期运动速度(e)及舒张早期充盈压（E/e）的变化。
4、统计学分析采用SPSS13.0统计软件，计量资料以均数±标准差（±s）
表示。两组资料比较用配对的t检验。P＜0.05为有统计学意义。结果
与初始时比较，标准乏氏动作张力期10秒时经二尖瓣血流速度E峰减低（P＜0.05），A峰没有变化（P＞0.05），E/A值减低（P＜0.05）；e没有变化（P＞0.05），E/e值减低（P＜0.05）。
结论
1，胸内正压对左室游离壁的力学作用阻碍了左室的舒张运动，引起E峰及E/A值减低；2，胸内正压降低了肺静脉系统与心脏的跨壁压力，增加了血流阻力也是导致肺静脉系统与左室血液回流减少，E峰减低，E/e值减低的一个原因。
第四部分：胸内正压对正常人左室收缩功能的直接影响及其力学机制
目的
应用超声心动图观测胸内正压对正常人左室收缩功能的直接影响并探讨其力学机制。
方法
1、实验对象
20名健康志愿者，男性15名，女性5名，平均年龄38.3岁（24-62岁）。入选条件：既往体健，无不良嗜好，体格适中，心电图、血压及心脏超声检查正常，检查前2小时内禁烟、酒、浓茶及咖啡。
2、仪器
2.1自制的乏氏动作负荷压定量装置。使用表式血压计改装而成，将原表式血压计袖带的一部分取下，接上一口鼻面罩，可将口鼻均罩入其内与外界大气隔离，使口腔、鼻腔与胸内气道压力一致。口鼻面罩的一个末端与压力表式指针相连，可定量与监测乏氏动作负荷压力。
2.2GE Vivid7彩色多普勒超声诊断仪，M3S探头，探头频率1.0～3.0MHz。
3、超声检查
所有测试均在晚上进行，至少晚饭后2小时。先瞩受试者平静呼吸，左后侧倾斜卧位，抬高左臂至枕后以伸展肋骨增大超声波透声窗，连接同步心电图，行常规超声心动图检查。观察心率呈稳定状态3分钟后记录并储存心尖四腔观或胸旁四腔观的二维超声及脉冲多普勒超声图像作为初始时的实验资料。然后瞩受试者捂紧气压测定装置的口鼻面罩做乏氏动作，要求呼气压在0.5秒之内达到40mmHg，在实时超声检查中存储受试者乏氏动作张力期心尖四腔观或胸旁四腔观的二维及脉冲多普勒超声图像。分析初始时与标准乏氏动作张力期10s时左室舒张末容积（LVEDV）、左室收缩末容积(LVESV)、每搏量(SV)、射血分值（EF）、心率（HR）、心输出量（CO）、主动脉最大血流速度（PV）及平均血流加速度（MAC）的变化。
4、统计学分析采用SPSS13.0统计软件，计量资料以均数±标准差（±s）
表示。两组资料比较用配对的t检验。P＜0.05为有统计学意义。
结果
与初始时比较，标准乏氏动作张力期10秒时LVEDV、LVESV及SV减低而HR增快（P均＜0.001），EF值增加，但无统计学意义（P＞0.05），CO及PV减低（P＜0.05），MAC没有变化，（P＞0.05）。
结论
胸内正压对左室游离壁的力学作用参与左室的收缩运动，其方向与左室本身的收缩力方向基本一致，两者合力增大，促进了左室的收缩运动，会引起EF值增加；胸内正常增加了血流阻力，引起回流量减低，导致SV、CO及PV减低。
Intrathoracic pressure changes with respiration, which exerts mechanicaleffects on cardiovascular hemodynamics. However, the mechanism of thisphenomenon still remains obscure. For over one hundred and thirty years, themechanism study for this phenomenon has challenged investigators and manyproposed hypotheses were proved to be irrational. Some have suggested thatinspiration increases venous capacitance of the pulmonary vessels, therebyreducing venous return to the left heart. But the results of the study by Scharf SMverified that without expansion of the pulmonary vessels, left heart output willstill decrease. Some have proposed that LV filling during inspiration decreasesbecause of compression of the LV from the enlarging right ventricle, however,this is just the description of the phenomenon but not the mechanism. It is alsoproposed that LV ejection is impeded by the fall of the intrathoracic pressurearound the heart comparable to an increase in arterial pressure, however, whichseems the consequence of decreased intrathoracic pressure and can notreasonably explain it.
We find that the above hypotheses failing to explain this phenomenon is that previous studies only involved the changes of LV hemodynamics and theresulting changes in LV function while neglected the directly mechanical effectsof intrathoracic pressure on LV ejection and filling. Accordingly, using theValsalva maneuver (VM) to simulate and amplify the situation of expiratoryphase, we designed these studies with echocardiography to evaluate the changesof LV ejection and filling induced directly by increased positive intrathoracicpressure.
Part1. Changes of left ventricular filling during the strain phase of Valsalvamaneuver in healthy subjects and its mechanism
Objective
The aim of this study was to explore changes of left ventricular filling duringthe strain phase of Valsalva maneuver (VM) and its mechanism.
Methods
30healthy volunteers were recruited to perform VM with a load of40mmHg.Left ventricular filling parameters (E, A, E/A ratio, e and E/e ratio) weredetermined by echocardiography at baseline, at the first beat and at the secondbeat during the strain phase of VM, respectively.
Results
Compared to those at baseline, E, E/A ratio and E/e ratio increased (P＜0.05）while A and e did not change (P＞0.05）at the first beat during the strain phase;Compared to those at the first beat during the strain phase, E, E/A ratio and E/eratio decreased (P＜0.05）while A and e did not change (P＞0.05）at the secondbeat during the strain phase.
Conclusions
Left ventricular filling decreased at the second beat during the strain phase of VM, which is different from the present knowledge that left ventricular fillingwould begin to decrease4-5beats later during the strain phase of VM. Positiveintrathoracic pressure decreases left-side heart and pulmonary vessel’ transmuralpressure while increases the blood resistance, which might be the reason that E,E/A ratio and E/e ratio decreased at the second beat during the strain phase ofVM.
Part2. Evaluation of the motion of septum during the strain phase ofValsalva maneuver in normal person by radius of curvature
Objective
The aim of this study was to evaluate the displacement of septum during thestrain phase of Valsalva maneuver (VM) in normal person by radius of curvature(RC).
Methods
23healthy volunteers were recruited to perform VM with a load of40mmHglasted for10seconds. The two-dimensional short-axis images of left ventricularduring quiet breath and during the VM were recorded and were analyzed withself-designed software to gain RC of septum and to calculate the changes.
Results
RC of septum during inspiration＞10th second during the VM＞duringexpiration＞5th second during the VM, any two of which, there is a significantchange (P＜0.01）.
Conclusions
During the strain phase of VM, septum will displace towards right ventricular at the5th second while there is no significant displacement at10th second.
Part3. Mechanical Effects of Positive Intrathoracic Pressure on LeftVentricular Filling in Healthy Subjects and Its Mechanism
Objective
Our aim was to explore the mechanical effects of positive intrathoracicpressure on left ventricular (LV) filling in healthy subjects and its mechanism.
Methods
1、 Subjects
We recruited thirty healthy volunteers,21men and9women, with a meanage of39±17years（range,23to66years), height of171±8cm, and weight of68±9kg in this study. None of these subjects had clinical symptoms, signs orhistory of any disease as determined by detailed inquiry, physical examination,electrocardiogram (ECG), chest X-ray and echocardiography. Alcohol, tobacco,strong tea and coffee were not allowed on the day of the test.
2、 Quantification of the load of VM
A self-made device was used to quantify and standardize the load of VM,which was modified from a watch style sphygmomanometer and has beendescribed in our previous study. Differently, a facial mask that could cut offventilation from both mouth and nose was used in the present study. Its functioncan compare with the previously used. All subjects were trained on how to usethe device to quantify and standardize a VM
3、 Examining protocol
At first, the subjects were asked to breathe quietly and naturally. After the subjects’ heart rate remaining at a stable level, echocardiography images wererecorded. Then the subjects were instructed to perform VM, at a load of40mmHg lasted for10seconds, with the self-made device quantified and standardized.Echocardiography images were recorded during the strain phase of VM.Measurements were performed at rest and at10th second during the strain phase.During measurements, investigators were blinded to the subjects’ data. HR wasobtained from the simultaneously recorded ECG. LV inflow velocities weredetermined using pulse-wave Doppler. Early diastolic flow velocity (E) and latediastolic flow velocity（A) were analyzed and E/A ratio was calculated. Earlydiastolic velocity (e) of the septal portion of the mitral annulus was determinedusing pulse-wave tissue Doppler imaging and E/e ratio was calculated.
4、 Statistics analysis
SPSS13.0statistic software was used. Data were expressed as mean±standard deviation. Continuous data were compared with paired Student’s t-testwhen appropriate. Probability ratio P＜0.05was considered statisticallysignificant.
Results
Compared to the rest, at10th second, early diastolic velocity (E)significantly decreased (P＜0.05), late diastolic velocity (A) insignificantlydecreased (P＞0.05) and E/A ratio significantly decreased (P＜0.05); earlydiastolic velocity (e) of the mitral annulus did not changed (P＞0.05) and E/eratio significantly decreased (P＜0.05), heart rate (HR) dramatically increased (P＜0.001).
Conclusions
Mechanical effect of positive intrathoracic pressure on LV free wall impedesLV diastolic motion, which could cause the decrease of E and E/A ratio. Positive intrathoracic pressure increases the flow resistance of LV and pulmonaryvasculature, which may contribute to the decrease of E and E/e ratio.
Part4. Mechanical Effects of Positive Intrathoracic Pressure on LeftVentricular systolic function in Healthy Subjects and Its Mechanism
Objective
Our aim was to explore the mechanical effects of positive intrathoracicpressure on left ventricular (LV) systolic function in healthy subjects and itsmechanism.
Methods
1、Subjects
We recruited twenty healthy volunteers,15men and5women, with a meanage of38.3years（range,24to62years). None of these subjects had the signs,symptoms, or history of disease as determined by history-taking, physicalexamination, electrocardiography (ECG), chest radiography, andechocardiography. Consumption of alcohol, tobacco, strong tea or coffee was notallowed on the test day.
2、Quantification of VM
A self-made device which was refitted from a watch-stylesphygmomanometer, as described in our previous study. A face-mask that couldcut off ventilation from the mouth and nose (and whose function could becompared with the face-mask used in our previous study) was employed. Allsubjects were trained on how to use the device to quantify and standardize a VM
2、Examining protocol
All experiments were undertaken in the evening≥2h after a light supper.GE Vivid7(GE Healthcare, Piscataway, NJ, USA) echocardiographic systemswere used with probe frequencies of2.5–4.0MHz.
Subjects were initially asked to breathe quietly and naturally. After a stableHR was achieved, echocardiographic images were recorded. Subjects were theninstructed to carry out the VM at a load of40mmHg for10s. This action wascarefully monitored using a self-made device. Echocardiographic images werealso recorded at10s during the strain phase. Measurements were recorded at restand at10s during the strain phase. During measurements, investigators wereblinded to the subjects’ data. Off-line analyses included left-ventricularend-diastolic volume (LVEDV), left-ventricular end-systolic volume (LVESV),stroke volume (SV), ejection fraction (EF), cardiac output (CO), peak aorticvelocity(PV) and mean local acceleration(MAC). HR was obtained from thesimultaneously recorded ECG.
4、 Statistics analysis
SPSS13.0statistical software (SPSS, Chicago, IL, USA) was used. Data aremean±standard deviation. Continuous data were compared using the pairedStudent’s t-test if appropriate. P＜0.05was considered significant.
Results
Compared to the rest, at10th second, LVEDV, LVESV and LV strokevolume (SV) dramatically decreased (P＜0.001) while heart rate (HR)dramatically increased (P＜0.001), and ejection fraction (EF) insignificantlyincreased (P＞0.05), CO and PV significantly decreased (P＜0.05), MAC hadnot changed (P＞0.05).Conclusions
Mechanical effects of positive intrathoracic pressure acts on LV free wall, itsdirection is nearly identical to that for the direction of the LV contraction force.Hence, cardiac systolic was enhanced and EF increased at10s during the strainphase of the VM. Mechanical effects of positive intrathoracic pressure increasesthe flow resistance of LV and pulmonary vasculature, which may contribute tothe decrease of blood volume, then the decrease of CO and PV.
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34. Henkind SJ, Benis AM, Teichholz LE. The paradox of pulsusparadoxus.Am Heart J.1987;114:198-203.
35. Fuenning C, Wise R, Brower R, et al. The mechanism of pulsusparadoxusin cardiac tamponade (abstract). Fed Proc.1985;44:1973.
36. Viola AR, Puy RJM, Goldman AE. Mechanisms of pulsus paradoxus inairway obstruction. J Appl Physiol.1990;68:1927-1931.
37. Klopfenstein H, Schuchard G, Wann L, et al. The relative merits of pulsusparadoxus and right ventricular diastolic collapse in the early detectionofcardiac tamponade: an experimental echocardiographic study.Circulation.1985;71:829-833.
38. Sun Y, Beshara M, Lucariello RJ, et al. A comprehensive model forright-left heart interaction under the influence of pericardium andbaroreflex.Am J Physiol.1997;272: H1499-H1515.
39. Tsang TS, Oh JK, Seward JB, et al. Diagnosis and management of cardiactamponade in the era of echocardiography. Clin Cardiol.1999;22:446-452.
40. Lange RL, Tsagaris TJ. Time course of factors causing exaggeratedrespiratory variation of arterial blood pressure. J Lab Clin Med.1964;63:
431.
41. Shabetai R, Fowler NO, Tenton J C. Pulsus paradoxus. J ClinInvest.1965;44:1882-1898.
42. Gabe IT, Mason DT, Gault JH, et al. Effects of respiration on venous returnand stroke volume in cardiac tamponade. Br. Heart J.1970;32:592.
43. Ruskin J, Bache RJ, Rembert JC, et al. Pressure flow studies in man: effectof respiration on left ventricular stroke volume. Circulation.1973;48:79.
44. Dornhorst AC, Howard P, Leathart GL. Pulsus paradoxus.Lancet.1952;1:746
45.曹铁生,袁丽君,段云友,等.胸压变化对两个静脉回流系统不同作用力学原理.第四军医大学学报.2002;23:1837-1840.
46. Cao T, Yuan L, Duan Y, et al. Mechanism study of Rispiration-relatedhemodynamics using in vitro and in vivo models. Circulation.2003;108:
1035.
47. Lijun Yuan, Tiesheng Cao, Yunyou Duan, et al. Noninvasive Assessmentof Influence of Resistant Respiration on Blood Flow Velocities across theCardiac Valves in Normal Man-a Quantification Study byEchocardiography. Echocardiography.2004;21:391-398.
48. Cao T,Yuan L,Duan Y.A novel noninvasive quantification method of leftventricular diastolic function. JACC.2007;4:213.
49. Scharf SM, Cassidy SS. Heart-lung interactions in health anddisease.Marcel Dekker, Inc;1989:445.
50. Mitchell JR, Sas R, Zuege DJ, Doig CJ, Smith ER, Whitelaw WA,TybergJV, Belenkie I. Ventricular interaction during mechanical ventilationinclosed-chest anesthetized dogs. Can J Cardiol2005;21(1):73-81.
51. Neumann P, Schubert A, Heuer J. Hemodynamic effects of spontaneousbreathing in the post-operative period. Acta Anaesthesiol Scand2005;49:1443-1448.
52. Miller JD, Smith CA, Hemauer SJ, Dempsey JA. The effects of inspiratoryintrathoracic pressure production on the cardiovascular response tosubmaximal exercise in health and chronic heart failure. Am J PhysiolHeart Circ Physiol2006;292: H580-H592.
53. Swami A, Spodick DH. Pulsus paradoxus in cardiac tamponade:apathophysiologic continuum. Clin. Cardiol2003;26(5):215-217.
54. Kasner M, Westermann D, Steendijk P, et al.Utility of Dopplerechocardiography and tissue Doppler imaging in the estimation of diastolicfunction in heart failure with normal ejection fraction:a comparativeDoppler-conductance catheterization study. Circulation.2007;116:637-647.
55. Persson H, Lonn E, Edner M, et al. Diastolic dysfunction in heart failurewith preserved systolic function: Need for objective evidence results fromthe CHARM echocardiographic substudy–CHARMES. J Am Coll Cardiol2007;49:687–94.
56. Zile MR, Baicu CF, Gaasch WH. Diastolic Heart Failure—Abnormalitiesin Active Relaxation and Passive Stiffness of the Left Ventricle. N Engl JMed.2004;350:1953-1959.
57. Ouzounian M, Lee DS, Liu PP. Diastolic heart failure: mechanisms andcontroversies. Nat Clin Pract Cardiovasc Med.2008;5:375-86.
58.袁丽君,曹铁生,段云友,等.平静呼吸对正常人心内血流速度影响的超声心动图研究.中华超声影像学杂志.2002;11:736-739.
59.李颖,曹铁生,袁丽君,等.平静呼吸对左室充盈的影响及其机制的超声心动图研究.中国超声医学杂志.2006;22:264-266.
60.李颖,曹铁生,袁丽君,等.平静呼吸对肺静脉血流的影响及其机制的超声心动图研究.中华超声影像学杂志.2006;15:51-54.
61.袁丽君,曹铁生,段云友,等.阻力呼吸对正常人血流动力学的影响及其临床意义研究.中华超声影像学杂志.2003;12:347-350.
62.袁丽君;曹铁生;段云友,等.心包积液时呼吸对血流动力学影响的超声心动图研究.中华超声影像学杂志.2004;13:96-99.
63.杨瑞静;曹铁生;段云友,等.呼吸对慢性阻塞性肺疾病心脏血流动力学影响的超声心动图研究.中华超声影像学杂志.2006;15:277-208.
64. Rebuck AS, Pengelly LD. Development of pulsus paradoxus in thepresence of airways obstruction. N Engl J Med.1973;288:66-69.
65. harpey-Schafer EP. Effect of respiratory acts on the circulation.In:Handbook of Physiology. Washington, DC: American PhysiologicalSociety;1965:1875–1886.
66. Haykowsky MJ, Eves ND, DE RW, et al. Resistance exercise, the Valsalvamaneuver, and cerebrovascular transmural pressure. Med Sci Sports Exerc.2003;35:65–68.
67. Rick A. Nishimura, A. Jamil Tajik, Rochester.The Valsalva Maneuver—3Centuries Later. Mayo Clin Proc,2004;79:577-578.
68. Khouri SJ, Maly GT, Suh DD, Walsh TE. A practical approach to theechocardiographic evaluation of diastolic function. J Am Soc Echocardiogr2004;17:290-297.
69. Ehud Schwammenthal, Bogdan A. Popescu, Andreea C. Popescu,Noninvasive Assessment of Left Ventricular End-Diastolic Pressure by theResponse of the Transmitral A-Wave Velocity to a Standardized ValsalvaManeuver Am J Cardiol2000;86:169–174.
70. Enilce Oliveira, Antonio L.P. Ribeiro, Fernando Assis Silva,et al. TheValsalva maneuver in Chagas disease patients without cardiopathy.International Journal of Cardiology.2002;82:49–54.
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