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1、心肺交互作用,首都醫(yī)科大學 北京朝陽醫(yī)院 李文雄,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,,PreloadTransmural pressure,跨壁壓（Ptm） 艙或血管內(nèi)外壓力差= 血管內(nèi)收縮壓 Ppl 非胸腔內(nèi)血管 外壓=大氣壓（傳

2、感器的零點） 胸腔內(nèi)血管 被胸膜腔內(nèi)壓包圍 胸膜腔內(nèi)壓隨通氣周期變化 Ppl RV前負荷 自主呼吸或負壓呼吸時Ppl 和血管內(nèi)主動脈壓力均下降 Ppl下降幅度大于主動脈壓力下降幅度 Ptm實際增加LV后負荷、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. Thi

3、s 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

4、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

5、 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 th

6、an 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

7、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 i

8、n 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 presen

9、ce 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

10、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 intralumin

11、al 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

12、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 potent

13、ial 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. Mechani

14、cal ven-tilation and acute cor pulmonale in Part II).,Intensive Care Med (2009) 35:4554,Afterload：effect of lung inflation,肺膨脹影響CO 肺膨脹擠壓肺泡內(nèi)血管 肺膨脹必須增加胸膜腔內(nèi)壓 PvPA時影響很小,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,

15、 based upon the relationship between the pressure in the alveoli (PA), in the arteries (Pa), and the veins (Pv):,Zones of the lung,肺動脈和靜脈壓力與肺部區(qū)域有關(guān) 肺尖最低 肺底最高 直立位肺頂部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.

16、J Appl Physiol 19: 71324.,Zones of the lung,全肺PA=02 cmH2O 直立位肺尖與肺底動脈壓差= 20 mmHg 受重力影響 全肺靜脈壓= 5 mmHg 肺尖部靜脈壓=-5 mmHg 肺底部靜脈壓= +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,正常人群全部肺區(qū)Pa PA Zone 1 正常情況下不存在 正壓通氣時可以存在 PAPa 受肺泡壓力影響區(qū)域血管徹底塌陷 血流消失 死腔通氣,Zones of the lu

17、ng,Zone 2 位于心臟上方 3cm以上肺區(qū) 區(qū)域血流呈搏動狀 毛細血管床靜脈端阻塞無血流 動脈端壓力超過PA時產(chǎn)生血流 如此反復循環(huán) 正常肺大部分位于Zone 3 存在連續(xù)血流 zone 1通氣/血流比 zone 3,Zones of the lung,PA Pv ( West zone II肺區(qū)) 右室后負荷隨肺膨脹增加 隨肺泡壓1 : 1 增加 肺血管血流淤滯肺水,The relation between lung volume and the pulmonary vascular resistance,As lung volume increases from residual v

18、olume (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 increasi

19、ng 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 volum

20、e,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 relationship

21、s 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

22、 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,正常靜脈回心反流梯度= 4 8 mmHg P

23、pl 小量增加可顯著改變靜脈回心反流梯度 Ppl 0時的兩種代償過程 增加血容量 補液 一段時間后腎臟鹽潴留代償機制發(fā)揮作用 靜脈容量血管收縮 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

24、 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

25、; 35:123 129.,For example,患者：中度肺疾病，PEEP=20 cmH2O Ppl可能增加8 cm H2O（ 約7 mmHg） 相對于大氣壓 CVP =15 mmHg 室壁膨脹壓=8 mmHg,For example,心臟水平外周毛細血管壓=15 mmHg 正常外周靜脈回心阻力=4 8 mmHg 外周靜脈靜水壓=19 23 mmHg 凈液體濾過到組織間隙 背側(cè)毛細血管額外靜水壓平均值= 7 cm 該部位外周靜脈靜水壓=2630mmHg 高的心臟充盈壓可能增加高PEEP患者CO 代價：血管內(nèi)血漿液體滲出增加,Model of the circulation showing

26、factors that influence systemic venous drainage,RH 和胸腔內(nèi)大靜脈受Ppl影響，并隨呼吸周期變化 吸氣時膈肌下降 IAP 呼氣時IAP正常（接近大氣壓） 外周靜脈壓不受呼吸周期影響 全身性靜脈回流 (broken arrow)取決于驅(qū)動壓（胸腔外大靜脈EGV壓-RAP） 自主吸氣時Ppl (RAP) ，IAP(EGV) ,Effects of increase in airway pressure and volume,Right ventricle Decreased preload Increased afterload Reduced c

27、ontractility 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 thereb

28、y 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,氣道壓力和容量對心臟負荷和功能的影響很復雜 對CO的影響取決于心臟和肺血管的基礎(chǔ)功能 Paw 對前負荷的影響通常占優(yōu) 右室后負荷損害性增加難以預測 血液動力學嚴重受損時應考慮 缺乏液體反應時應考慮 Echocardiograp

29、hy 可指導治療 應考慮心肺交互作用對臨床表現(xiàn)和治療的影響,Hemodynamic monitoringBlood pressure,BP （隨呼吸機設置變化） 意味著 CO 、組織氧合 需要恢復先前通氣設置 呼吸正壓 而BP沒有下降并不意味著CO沒有下降 CO 時神經(jīng)-體液反射能迅速增加SRV以維持或增加BP BP 檢測CO變化特異性高，敏感性低,Hemodynamic monitoringCVP,CVP 不表示血容量 CVP 不能表示容量反應性 一個特定的CVP值不表明患者是否具有容量反應性 高CVP表明患者不太可能具有容量反應性 CVP 10 12mmHg,Hemodynamic mon

30、itoringCVP,應用CVP時首先要基于臨床和生化檢查來判斷患者是否需要優(yōu)化血液動力學 其次是快速補液是否改善血液動力學 最后是當CVP隨擴容增加時是否能增加CO CVP應在一定的安全范圍內(nèi),Hemodynamic monitoringCVP,For example 患者：中度肺疾病，PEEP=20 cmH2O Ppl可能增加8 cm H2O（ 約7 mmHg） 相對于大氣壓 CVP =15 mmHg 室壁膨脹壓=8 mmHg,Hemodynamic monitoringCVP,心臟水平外周毛細血管壓=15 mmHg 外周靜脈回心阻力=4 8 mmHg 外周靜脈靜水壓=19 23 mmHg

31、 凈液體濾過到組織間隙 背側(cè)毛細血管額外靜水壓平均值= 7 cm 該部位外周靜脈靜水壓=2630mmHg 高的心臟充盈壓可能增加高PEEP患者CO 代價：血管內(nèi)血漿液體滲出增加,,存在較大肺分流時，低CO影響PaO2 CO SvO2 CaO2 監(jiān)測SvO2 or ScvO2有用 SvO2 or ScvO2很低表明增加CO將增加PaO2,Diagnostic uses of ventilatory variation in vascular pressure waves-Respiratory variations in central venous pressure,Interaction

32、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 與 PAOP 可用來評價通氣功能 PAOP 通氣變異度可表明Ppl的變化27. 自主負壓吸氣時，PAOP 下降輕度低估了Ppl的下降 大多數(shù)病人肺充氣時左室充盈增加 正壓呼吸時，PAOP增加輕度高估了Ppl的

33、增加,Evaluation of respiratory function,CVP的變化基本不反應Ppl的變化 右心容量來源于胸腔外 基本不隨Ppl而變化 吸氣觸發(fā)時 CVP or PAOP出現(xiàn)大的負向變化 trigger 設置不當 Raw 肺順應性 吸氣驅(qū)動增強 需調(diào)整通氣設置或增強鎮(zhèn)靜,Evaluation of respiratory function,CVP隨MV顯著增加 表明Ppl 顯著增加 胸壁順應性 胸壁水腫 胸腔積液量大 IAP增加,Evaluation of respiratory function,用力呼氣使CVP增高 需觀察多個呼吸周期 取呼氣末獲得值（最長和最低值） (

34、Fig. 3b) 呼氣階段患者增加收縮呼氣肌時，整個呼氣階段心臟充盈壓增加(Fig. 3c) 這些患者CVP 呼氣末值誤導前負荷的估價 取呼氣開始時的CVP值可能更有效 患者試圖談話時消失 氣管插管降低呼氣肌收縮后消失,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,對于簡單的MV患者間斷觀察BP和SpO2足夠了 通氣管理很困難時

35、 監(jiān)測血液動力學 試圖增加PaO2時需評價CO以保證MV不降低DO2 從CVP和BP波形可獲得很多信息指導治療,Using heartlung interactions to assess fluid responsiveness during mechanical ventilation,Respiratory variations in arterial pressure and stroke volume,控制通氣吸氣段 Ppl 靜脈回心梯度 RV充盈和CO BP 肺充氣 肺靜脈排空 LV充盈增加LV CO Ppl LV后負荷 控制通氣呼氣段 BP SV,Respiratory cha

36、nges 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

37、,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 circula

38、tory 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

39、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, 159:9359

40、39.,,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

41、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,Hemody

42、namic 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 intensiv

43、e 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 posi

44、tive 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

45、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 spo

46、ntaneous ventilation to optimize the likelihood of success,,謝謝,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 gre

47、at 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 pres

48、sure 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,

49、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. Convers

50、ely, 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.,The relation between lung volume and the pulmonary vascular resistance,As

51、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) f

52、alls. 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.,,If the healthy cardiopulmonary system is ventilated near “normal” FRC without exces-sive shifts in lung volume, it is unusual to see clinically important changes in RV afterload with a PEEP of less than 10 cm H2O.,