心肺交互作用simplified.ppt

心肺交互作用1Basic physiology of heartlung interactionPump function:Preload at a given HRPra or CVPAfterload Contractility.Return function:Blood volume(vein)stressed and unstressedComplianceResistanceCO2PreloadTransmural 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 3Four 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.20094Ventricular afterloadDefinition:the force opposing ejectionVentricular 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.5LV afterloadAt 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 6RV afterloadA 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 PAFor 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)35:45547Afterload：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PvPA时影响很小8Zones of the lungZone 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):9Zones 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PAWest J,Dollery C,Naimark A(1964).Distribution of blood flow in isolated lung;relation to vascular and alveolar pressures.J Appl Physiol 19:71324.10Zones 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 11Zones of the lung正常人群全部肺区Pa PAZone 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12Zones of the lungZone 2 Zone 2 位于心脏上方位于心脏上方 3cm 3cm以上肺区以上肺区 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正常肺大部分位于Zone 3Zone 3存在连续血流zone 1通气/血流比 zone 313Zones of the lungPA 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14The relation between lung volume and the pulmonary vascular resistanceAs 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;15:87882.15FrankStarling relationships between ventricular preload and stroke volumeA 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).16FrankStarling relationships between ventricular preload and stroke volumeSchematic 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.17Return functionHeartstressed volumeUnstressed volumeHeight:Total BVEmptying BVResistanceCompliance:Surface/HeightrelationshipReturn function:Blood volume(veins/venules)stressed and unstressedComplianceResistance18Return function正常静脉回心反流梯度=4 8 mmHgPpl 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/kg19Return functionUnstressed volumeStressed volumeStressed volumeUnstressed volumeContraction of smooth muscle in vascular wallsReturn to heart 20the 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)valuesGuyton AC.Determination of cardiac output by equating venous return curves with cardiac response curves.Physiol Rev 1955;35:123 129.21 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 mmHg22For 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23Model of the circulation showing factors that influence systemic venous drainageRH 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)24Effects of increase in airway pressure and volumeRight ventricleDecreased preloadIncreased afterloadReduced contractilityCompression of heart in cardiac fossaLeft ventricleDecreased preloadDecreased complianceVariable effects on(autonomous nervous system control of)contractilityDecreased afterloadCompression of heart in cardiac fossaMechanical ventilation alters intrathoracic pressures and thereby affects the cardiovascular system,mainly the right ventricle25Cardiovascular effects of mechanical ventilation and application of PEEP26Effects 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27Hemodynamic monitoringBlood pressureBP （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BPBP 检测CO变化特异性高，敏感性低28Hemodynamic monitoringCVPCVP 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 12mmHg29Hemodynamic 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COCVP应在一定的安全范围内30Hemodynamic 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 mmHg31Hemodynamic 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32存在较大肺分流时，低CO影响PaO2CO SvO2 CaO2 监测SvO2 or ScvO2有用SvO2 or ScvO2很低表明增加CO将增加PaO233Diagnostic uses of ventilatory variation in vascular pressure waves-Respiratory variations in central venous pressureInteraction of venous return and cardiac function curves with respiratory variation34Interaction of venous return and cardiac function curves with respiratory variations35Evaluation 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36Evaluation of respiratory functionCVP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37Evaluation of respiratory functionCVP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38Evaluation 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39Example of pulmonary artery occlusion pressure(Ppao),a reflection of left atrial pressure,and CVP in a patient on a pressure support of 6 cmH2O40Conclusion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41Using heartlung interactions to assess fluid responsiveness during mechanical ventilation42Respiratory 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BPSV43Respiratory 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+CVP44Using heartlung interactions to assess fluid responsiveness during mechanical ventilationRelationship 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 2000,162:13413845Using heartlung interactions to assess fluid responsiveness during mechanical ventilationRelationship 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 1999,159:935939.4647Using heartlung interactions to assess fluid responsiveness during mechanical ventilation48Using heartlung interactions to assess fluid responsiveness during mechanical ventilation4950Using heartlung interactions to assess fluid responsiveness during mechanical ventilationMichard F.Am J Respair Crit Care Med 1999;159:935939.51Determinants of pulse variation52Ventilatory 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 24,25,2653Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients54Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients55Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients56Hemodynamic changes during discontinuation of machanical ventilation in medical intensive care unit patients57Patterns 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;15:580-59458summaryEffects of increase in airway pressure and volume on right and left ventricleHeart-lung interactions may play a role in the manifestations and treatment of a variety of disordersUsing heartlung interactions (PPV)can assess fluid responsiveness during mechanical ventilationCardiac function must be systematically considered before and during the return to spontaneous ventilation to optimize the likelihood of success59谢谢60Hypoxic pulmonary vasoconstriction in human lungsAnaesthesiology 1997,86:308-31561Hypoxic pulmonary vasoconstriction in human lungs62Model of the circulation showing factors that influence systemic venous drainageRH 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 rises63Negative 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 can reduce or overcome“negative inspiratory swings”in intrathoracic pressure,and by lowering the afterload,will potentially restore the haemodynamics to a more favourable position on the Starling curve.64The relation between lung volume and the pulmonary vascular resistanceAs 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