心肺交互作用.ppt

,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,心肺交互作用,Basic physiology of heartlung interaction,Pump function:,Preload at a given HR,Pra or CVP,Afterload,Contractility.,Return function:,Blood volume(vein),stressed and unstressed,Compliance,Resistance,CO,Preload,Transmural pressure,跨壁压（,Ptm,）,舱或血管内外压力差,=,血管内收缩压,Ppl,非胸腔内血管,外压,=,大气压（传感器的零点）,胸腔内血管,被胸膜腔内压包围,胸膜腔内压随通气周期变化,Ppl,RV,前负荷,自主呼吸或负压呼吸时,Ppl,和血管内主动脉压力均下降,Ppl,下降幅度大于主动脉压力下降幅度,Ptm,实际增加,LV,后负荷、,SV,Four mechanisms participate in the cyclic changes of SV observed during mechanical ventilation.,First,during insufflation,venous return decreases due to an increase in pleural pressure.This decrease in RV preload leads to a decrease in RV output that subsequently leads to a decrease in left ventricular output.Second,RV afterload increases during inspiration because the increase in alveolar pressure is greater than the increase in pleural pressure.,However,left ventricular preload in-creases during insufflation because blood is expelled from the capillaries toward the left atrium.,Finally,left ventricular afterload decreases during inspiration because positive pleural pressure decreases the intracardiac systolic pressure and the transmural pressure of the intrathoracic part of the aorta,CCM.2009,Ventricular afterload,Definition:the force opposing ejection,Ventricular afterload is represented by the level of transmural pressure,in the course of systole,within either the aortic root(LV afterload)or the pulmonary artery trunk(RV after-load),The transmural rather than the intraluminal pressure must be considered because these great vessels as well as the ventricles are exposed to an extramural pressure(i.e.,ITP)which is usually non atmospheric.,The mechanisms whereby respiration interacts with LV and RV afterload are different.,LV afterload,At the onset of spontaneous inspiration,the intraluminal pressure in the aortic root decreases less than does ITP,due to the connection of this vessel with extrathoracic arteries.As a result,aortic transmural pressure increases.,With spontaneous breathing therefore,LV afterload is greater in inspiration than in expiration.A symmetrical chain of events leads to a reduced LV afterload in the course of a transient increase in ITP,such as with positive pressure inflation of the lungs.Steady increases in ITP,as effected with PEEP,similarly unload the LV with potentially beneficial consequences in presence of left heart failure,as described in greater detail below(Sect.Effects of PEEP on cardiac output in Part II).,Conversely,patients with obstructive sleep apnea have bouts of greatly negative ITP which increase LV after-load,thus contributing to LV hypertrophy,RV afterload,A seminal paper by Permutt shows that RV afterload is highly dependent on and increases with the proportion of lung tissue in West zone 1 or 2,as opposed to zone 3 conditions.Zones 1 or 2 exist whenever the extraluminal pressure of alveolar capillaries(which is close to alveolar pressure,PA)exceeds the intraluminal value,leading to vessel compression.In zone 3 by contrast,intraluminal capillary pressure exceeds PA,For hydrostatic reasons,zones 1 and 2 are more likely to occur in nondependent parts of the lung.Furthermore,respiratory changes in the intraluminal pressure of alveolar capillaries tend to track changes in ITP and thus to decrease more than does PA during a spontaneous inspiration and to increase less than does PA on inflation of the lung with positive pressure.Thus,any increase in lung volume,whether in the context of spontaneous or mechanically assisted breathing,has the potential to promote the formation of zones 1 and 2 at the expense of zone 3,and thus to increase RV afterload.These considerations are of high clinical relevance,notably concerning the possible induction or aggravation of acute cor pulmonale by mechanical ventilation,as described below(Sect.Mechanical ven-tilation and acute cor pulmonale in Part II).,Intensive Care Med(2009)35:4554,Afterload,：,effect of lung inflation,肺膨胀影响,CO,肺膨胀挤压肺泡内血管,肺膨胀必须增加胸膜腔内压,Pv,PA,时影响很小,Zones of the lung,Zone 1:PA Pa Pv,Zone 2:Pa PA Pv,Zone 3:Pa Pv PA,The,zones of the lung,divide the,lung,into three vertical regions,based upon the relationship between the pressure in the,alveoli,(PA),in the,arteries,(Pa),and the,veins,(Pv):,Zones of the lung,肺动脉和静脉压力与肺部区域有关,肺尖最低,肺底最高,直立位肺顶部,Pa,很可能低于,PA,West J,Dollery C,Naimark A(1964).Distribution of blood flow in isolated lung;relation to vascular and alveolar pressures.,J Appl Physiol,19,:71324.,Zones of the lung,全肺,PA=02 cmH2O,直立位肺尖与肺底动脉压差,=20 mmHg,受重力影响,全肺静脉压,=5 mmHg,肺尖部静脉压,=-5 mmHg,肺底部静脉压,=+15 mmHg,PAP=25/10 mmHg,（,Mean=15 mmHg,）,肺尖部,mPAP=5 mmHg,肺底部,mPAP=25 mmHg,Zones of the lung,正常人群全部肺区,Pa PA,Zone 1,正常情况下不存在,正压通气时可以存在,PAPa,受肺泡压力影响区域血管彻底塌陷,血流消失,死腔通气,Zones of the lung,Zone 2,位于心脏上方,3cm,以上肺区,区域血流呈搏动状,毛细血管床静脉端阻塞,无血流,动脉端压力超过,PA,时产生血流,如此反复循环,正常肺大部分位于,Zone 3,存在连续血流,zone 1,通气,/,血流比,zone 3,Zones of the lung,PA Pv(West zone II,肺区,),右室后负荷随肺膨胀增加,随肺泡压,1:1,增加,肺血管血流淤滞,肺水,The,relation between lung volume and the pulmonary vascular resistance,As lung volume increases from residual volume(RV)to total lung capacity(TLC),the alveolar vessels become increasingly compressed by the distending alveoli,and so their resistance increases,whereas the resistance of the extra-alveolar vessels(which become less tortuous as lung volume increases)falls.,The combined effect of increasing lung volume on the pulmonary vasculature produces the typical“U shaped”curve as shown,with its nadir,or optimum,at around normal functional residual capacity(FRC).,Whittenberger JL,et al.,J Appl Physiol 1960;15:87882.,FrankStarling relationships between ventricular preload and stroke volume,A given change in preload induces a larger change in stroke volume when the ventricle operates on the ascending portion of the relationship(A,condition of preload dependence)than when it operates on the flat portion of the curve(B,condition of preload independence).,FrankStarling relationships between ventricular preload and stroke volume,Schematic representation of FrankStarling relationships between ventricular preload and stroke volume in a normal heart(A)and in a failing heart(B).A given value of preload can be associated with preload dependence in a normal heart or with preload independence in a failing heart.,Return function,Heart,stressed volume,Unstressed volume,Height:,Total BV,Emptying BV,Resistance,Compliance:,Surface/Height,relationship,Return function:,Blood volume(veins,/venules,),stressed and unstressed,Compliance,Resistance,Return function,正常静脉回心反流梯度,=4 8 mmHg,Ppl,小量增加可显著改变静脉回心反流梯度,Ppl,0,时的两种代偿过程,增加血容量,补液,一段时间后肾脏盐潴留代偿机制发挥作用,静脉容量血管收缩,Unstressed stressed volume stressed volume,迅速增加,stressed volume 1015 ml/kg,Return function,Unstressed volume,Stressed,volume,Stressed volume,Unstressed,volume,Contraction of smooth muscle in vascular walls,Return to heart,the interaction of venous return curve(upper left)and cardiac function curve(upper right)define the working cardiac output,venous return and right atrial pressure(Pra)values,Guyton AC.Determination of cardiac output by equating venous return curves with cardiac response curves.Physiol Rev 1955;35:123 129.,For example,患者：中度肺疾病，,PEEP=20 cmH2O,Ppl,可能增加,8 cm H2O,（,约,7 mmHg,）,相对于大气压,CVP=15 mmHg,室壁膨胀压,=8 mmHg,For example,心脏水平外周毛细血管压,=15 mmHg,正常外周静脉回心阻力,=4 8 mmHg,外周静脉静水压,=19 23 mmHg,净液体滤过到组织间隙,背侧毛细血管额外静水压平均值,=7 cm,该部位外周静脉静水压,=2630mmHg,高的心脏充盈压可能增加高,PEEP,患者,CO,代价：血管内血浆液体渗出增加,Model of the circulation showing factors that influence systemic venous drainage,RH,和胸腔内大静脉受,Ppl,影响，并随呼吸周期变化,吸气时膈肌下降,IAP,呼气时,IAP,正常（接近大气压）,外周静脉压不受呼吸周期影响,全身性静脉回流,(broken arrow),取决于驱动压（胸腔外大静脉,EGV,压,-RAP,）,自主吸气时,Ppl(RAP),，,IAP(EGV),Effects of increase in airway pressure and volume,Right ventricle,Decreased preload,Increased afterload,Reduced contractility,Compression of heart in cardiac fossa,Left ventricle,Decreased preload,Decreased compliance,Variable effects on(autonomous nervous system control of)contractility,Decreased afterload,Compression of heart in cardiac fossa,Mechanical ventilation alters intrathoracic pressures and thereby affects the cardiovascular system,mainly the right ventricle,Cardiovascular effects of mechanical ventilation and application of PEEP,Effects of increase in airway pressure and volume,气道压力和容量对心脏负荷和功能的影响很复杂,对,CO,的影响取决于心脏和肺血管的基础功能,Paw,对前负荷的影响通常占优,右室后负荷损害性增加难以预测,血液动力学严重受损时应考虑,缺乏液体反应时应考虑,Echocardiography,可指导治疗,应考虑心肺交互作用对临床表现和治疗的影响,Hemodynamic monitoringBlood pressure,BP,（随呼吸机设置变化）,意味着,CO,、组织氧合,需要恢复先前通气设置,呼吸正压,而,BP,没有下降并不意味着,CO,没有下降,CO,时神经,-,体液反射能迅速增加,SRV,以维持或增加,BP,BP,检测,CO,变化特异性高，敏感性低,Hemodynamic monitoringCVP,CVP,不表示血容量,CVP,不能表示容量反应性,一个特定的,CVP,值不表明患者是否具有容量反应性,高,CVP,表明患者不太可能具有容量反应性,CVP,10 12mmHg,Hemodynamic monitoringCVP,应用,CVP,时首先要基于临床和生化检查来判断患者是否需要优化血液动力学,其次是快速补液是否改善血液动力学,最后是当,CVP,随扩容增加时是否能增加,CO,CVP,应在一定的安全范围内,Hemodynamic monitoringCVP,For example,患者：中度肺疾病，,PEEP=20 cmH2O,Ppl,可能增加,8 cm H2O,（,约,7 mmHg,）,相对于大气压,CVP=15 mmHg,室壁膨胀压,=8 mmHg,Hemodynamic monitoringCVP,心脏水平外周毛细血管压,=15 mmHg,外周静脉回心阻力,=4 8 mmHg,外周静脉静水压,=19 23 mmHg,净液体滤过到组织间隙,背侧毛细血管额外静水压平均值,=7 cm,该部位外周静脉静水压,=2630mmHg,高的心脏充盈压可能增加高,PEEP,患者,CO,代价：血管内血浆液体渗出增加,存在较大肺分流时，低,CO,影响,PaO2,CO SvO2 CaO2,监测,SvO2 or ScvO2,有用,SvO2 or ScvO2,很低表明增加,CO,将增加,PaO2,Diagnostic uses of ventilatory variation in vascular pressure waves-Respiratory variations in central venous pressure,Interaction of venous return and cardiac function curves with respiratory variation,Interaction of venous return and cardiac function curves with respiratory variations,Evaluation of respiratory function,CVP,与,PAOP,可用来评价通气功能,PAOP,通气变异度可表明,Ppl,的变化,27.,自主负压吸气时，,PAOP,下降轻度低估了,Ppl,的下降,大多数病人肺充气时左室充盈增加,正压呼吸时，,PAOP,增加轻度高估了,Ppl,的增加,Evaluation of respiratory function,CVP,的变化基本不反应,Ppl,的变化,右心容量来源于胸腔外,基本不随,Ppl,而变化,吸气触发时,CVP or PAOP,出现大的负向变化,trigger,设置不当,Raw,肺顺应性,吸气驱动增强,需调整通气设置或增强镇静,Evaluation of respiratory function,CVP,随,MV,显著增加,表明,Ppl,显著增加,胸壁顺应性,胸壁水肿,胸腔积液量大,IAP,增加,Evaluation of respiratory function,用力呼气使,CVP,增高,需观察多个呼吸周期,取呼气末获得值（最长和最低值）,(Fig.3b),呼气阶段患者增加收缩呼气肌时，整个呼气阶段心脏充盈压增加,(Fig.3c),这些患者,CVP,呼气末值误导前负荷的估价,取呼气开始时的,CVP,值可能更有效,患者试图谈话时消失,气管插管降低呼气肌收缩后消失,Example of pulmonary artery occlusion pressure(Ppao),a reflection of left atrial pressure,and CVP in a patient on a pressure support of 6 cmH2O,Conclusion,对于简单的,MV,患者间断观察,BP,和,SpO2,足够了,通气管理很困难时,监测血液动力学,试图增加,PaO2,时需评价,CO,以保证,MV,不降低,DO2,从,CVP,和,BP,波形可获得很多信息指导治疗,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Respiratory variations in arterial pressure and stroke volume,控制通气吸气段,Ppl ,静脉回心梯度,RV,充盈和,CO,BP,肺充气 肺静脉排空,LV,充盈增加,LV CO,Ppl LV,后负荷,控制通气呼气段,BP,SV,Respiratory changes in airway and arterial pressures in a mechanically ventilated patient,The pulse pressure(systolic minus diastolic pressure)is maximal(PPmax)at the end of the inspiratory period and minimal(PPmin)three heart beats later(ie during the expiratory period).,SVRI=CI/(MAP-CVP),MAP=CI/SVRI+CVP,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Relationship between the respiratory changes in pulse pressure before volume expansion(Baseline,；,PP)and the volume expansion-induced changes in cardiac index(,y-axis)in 40 septic patients with acute,circulatory failure.The higher,PP is before volume expansion,the more marked the increase in cardiac index induced by volume expansion.,Michard F.Am J Respir Crit Care Med 2000,162:134138,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Relationship between the respiratory changes in pulse pressure on ZEEP(,y-axis)and the PEEP-induced changes in cardiac index(x-axis),in 14 ventilated patients with acute lung injury.The higher,PP is on ZEEP,the more marked the decrease in cardiac index induced by PEEP.,Michard F.Am J Respir Crit Care Med 1999,159:935939.,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Michard F.Am J Respair Crit Care Med 1999;159:935939.,Determinants of pulse variation,Ventilatory variations in arterial pressure or stroke volume have also been shown not to be predictive in patients with smaller tidal volumes,increased West zone II conditions and in patients with pulmonary hypertension 24,25,26,Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients,Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients,Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients,Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients,Patterns of cardiac function and plasma catecholamine levels differed between patients who did or did not achieve spontaneous ventilation with a trial of continuous positive airway pressure.,Cardiac function must be systematically considered before and during the return to spontaneous ventilation to optimize the likelihood of success.,Susan KF.American Journal of Critical Care.2006;15:580-594,summary,Effects of increase in airway pressure and volume on right and left ventricle,Heart-lung interactions may play a role in the manifestations and treatment of a variety of disorders,Using heartlung interactions (PPV)can assess fluid responsiveness during mechanical ventilation,Cardiac function must be systematically considered before and during the return to spontaneous ventilation to optimize the likelihood of success,谢谢,Hypoxic pulmonary vasoconstriction in human lungs,Anaesthesiology 1997,86:308-315,Hypoxic pulmonary vasoconstriction in human lungs,Model of the circulation showing factors that influence systemic venous drainage,RH and intrathoracic great veins are subjected to pleural pressure(PPl),which varies throughout the respiratory cycle.IAP increases with inspiratory diaphragmatic descent,and normalises to atmospheric(Patmos)with expiration.,Peripheral venous pressure is unaffected by respiration and so remains at atmospheric pressure throughout the respiratory cycle.,Systemic venous drainage(broken arrow)depends on a driving pressure gradient between extrathoracic great veins(EGV)and the right atrium,and so during spontaneous respiration is maximised during inspiration as the pleural(and right atrial)pressure falls,and the intra-abdominal(and therefore EGV)pressure rises,Negative swings in intrathoracic pressure for example,during a Mueller manoeuvre(deep inspiration against a closed glottis),or the discontinuation of PPV can cause acute increases in afterload in the presence of poor LV function.,Conversely,PPV with PEEP