進(jìn)入讀到了刊登于Pulmccm Journal的2014年第9期的《The Pathomechanics of Extubation Failure A Clinical Review》后，我覺(jué)得有必要介紹給大家、

The Pathomechanics of Extubation Failure A Clinical Review

Jon-Emile Kenny MD

September 27, 2014 · 

鏈接：http:///journal/article/the-pathomechanics-of-extubation-failure/

摘要：

通常認(rèn)為已通過(guò)“自主呼吸試驗(yàn)”的患者能很好地耐受因機(jī)械通氣撤離引起的生理變化。然而確實(shí)存在一小部分患者，他們盡管在非常低的呼吸機(jī)支持下呼吸負(fù)荷是可接受的，但在移除氣管插管后會(huì)發(fā)生心肺功能障礙（及心肺崩潰）。這些患者通常具有潛在的并發(fā)性心肺疾病使得生理儲(chǔ)備不足，這即可由任一器官系統(tǒng)誘發(fā)，也可因其他長(zhǎng)期存在的病理生理異常所致。 了解這些有害的相互作用可能有助于臨床醫(yī)生發(fā)現(xiàn)拔管后的心臟呼吸負(fù)荷異常和血液動(dòng)力學(xué)的窘境。

The physiological changes induced by liberation from mechanical ventilation are usually well tolerated by patients deemed to have passed a “spontaneous” breathing trial. However, a subset of patients with acceptable indices of respiratory load while on very low ventilator support will subsequently experience cardiopulmonary collapse following removal of the endotracheal tube. These patients typically have underlying co-morbid cardiopulmonary disease whereby poor physiological reserve in either organ system induces and perpetuates pathophysiology in the other. Knowledge of these deleterious interactions may help the clinician anticipate abnormal cardio-respiratory load and hemodynamic embarrassment after extubation.

介紹

胸部和位于其內(nèi)的心臟各自周期性地改變其壓力和體積，并且兩者之間存在不可避免的機(jī)械聯(lián)動(dòng)。 壓力和體積是胸部從物理上改變雙心室前負(fù)荷和后負(fù)荷的兩個(gè)主要變量。 疾病與健康時(shí)呼吸負(fù)荷，胸內(nèi)壓力和容量之間的關(guān)系可以在坎貝爾圖上顯示（圖1）。

The thorax and the heart within in it each vary their pressures and volumes cyclically, and there is an inescapable mechanical linkage between the two. Pressure and volume are the two dominant variables by which the thorax physically alters biventricular preload and afterload.1 The relationship between respiratory loads, intrathoracic pressure and volume in sickness and in health can be shown on a Campbell diagram (Figure 1).

圖1.坎貝爾圖說(shuō)明呼吸負(fù)荷，胸腔內(nèi)壓力和體積之間的關(guān)系

當(dāng)患者從機(jī)械通氣中撤離時(shí)，呼吸系統(tǒng)的彈性和阻力負(fù)荷增大；這在之前就有肺部疾病的患者中變得特別顯著。自主呼吸的努力可能會(huì)產(chǎn)生夸張的胸內(nèi)壓力和體積的波動(dòng)，對(duì)心血管系統(tǒng)形成牽張，進(jìn)而增加呼吸負(fù)荷。 由心血管系統(tǒng)，呼吸系統(tǒng)的病理生理學(xué)或兩者的組合引起和持續(xù)的異?？梢越忉屇承┗颊邚臋C(jī)械通氣移除后的病情快速惡化。知曉這些有害的相互作用可能有助于臨床醫(yī)生在將患者從呼吸機(jī)解放之前能夠預(yù)期并糾正心肺負(fù)荷的攪擾。

本綜述不會(huì)討論機(jī)械通氣向自發(fā)通氣過(guò)渡是并發(fā)的的神經(jīng)激素和自主神經(jīng)的異常。 綜述中列出的呼吸生理概念可在作者網(wǎng)站（ www.heart-lung.org ）的在線附錄內(nèi)容中進(jìn)一步查閱。

When a patient is removed from mechanical ventilation, the elastic and resistive loads of the respiratory system are augmented; this becomes especially pronounced in patients with preexisting pulmonary pathology.2 Spontaneous breathing efforts may generate exaggerated swings in intrathoracic pressure and volume that stress the cardiovascular system and in turn increase respiratory load. The means by which pathophysiology in the cardiovascular system, respiratory system or a combination of the two initiate and perpetuate abnormalities in each other can explain the rapid deterioration seen in some patients following removal from mechanical ventilation.3 Knowledge of these injurious interactions may help the clinician anticipate and correct perturbations in cardiorespiratory load prior to liberating a patient from the ventilator.

This review will not discuss the neurohormonal and autonomic abnormalities that complicate the transition from mechanical ventilation to spontaneous ventilation.4 The concepts in respiratory physiology outlined here are reviewed further in the online supplement at the author’s website (www.heart-lung.org).

呼吸負(fù)荷：氣道阻力和胸部順應(yīng)性

呼吸系統(tǒng)負(fù)荷通常分為動(dòng)態(tài)和靜態(tài)部分。這些呼吸生理都在坎貝爾圖上顯示，并且將依次討論，隨后。將討論當(dāng)患者從呼吸機(jī)解放時(shí)可能出現(xiàn)的病理生理負(fù)荷。

The load placed upon the respiratory system is typically divided into dynamic and static components. Each of these aspects of respiratory physiology are represented on the Campbell diagram and will be discussed in turn, followed by discussion of the pathophysiological load which may arise when a patient is liberated from the ventilator.

動(dòng)態(tài)呼吸壓力

氣管支氣管樹中的氣流可依照電流的歐姆定律模型。 從數(shù)學(xué)上講阻力可由壓力和流量的關(guān)系定義。 阻力模型可預(yù)測(cè)壓力和流量之間的線性關(guān)系，但在氣管支氣管中壓力 -流量關(guān)系在高流量時(shí)會(huì)”“彎曲”，這是因?yàn)楫a(chǎn)生了一過(guò)性的湍流，其要比層流形成更高的有效阻力。層流可以被認(rèn)為是氣體分子在同心排列的拋物線中的有序流動(dòng)運(yùn)動(dòng)，最內(nèi)分子以最高速度流動(dòng)。

氣道阻力或流動(dòng)模式的變化改變了胸膜壓力的絕對(duì)值。 在自發(fā)呼吸的患者中，動(dòng)態(tài)壓力的性質(zhì)被描繪為肺靜態(tài)壓力 - 體積關(guān)系左側(cè)的曲線（圖2）。

Ohm’s law of electrical current is the model after which gas flow within the tracheobronchial tree is typically modeled. Resistance is defined mathematically by the relationship of pressure and flow. This model of resistance predicts a linear relationship between pressure and flow, but in the tracheobronchial tree, the pressure-flow relationship “bends” at high flows because of the production of transitional and turbulent flows which have higher effective resistances than laminar flow.7,8 Laminar flow can be thought of as an orderly flowing motion of gas molecules in concentrically arranged parabolas with the innermost molecules flowing with the highest velocity.

Changes in airways resistance or flow pattern alter absolute values of pleural pressure. In the spontaneously breathing patient, dynamic pressure properties are depicted as a curve to the left of the static pressure-volume relationship of the lung (figure 2).

圖2.胸膜壓力的變化（由于氣道阻力，流量等）導(dǎo)致肺順應(yīng)性曲線的變化

靜態(tài)呼吸壓力

呼吸中的靜壓力代表影響肺和胸腔體積變化所需的胸內(nèi)壓力，它與氣體流動(dòng)無(wú)關(guān)。 這種壓力可以由感興趣容量的靜態(tài)肺和胸壁順應(yīng)性曲線之間的橫向距離來(lái)表示（圖3）。

The static pressure invested in respiration represents the intrathoracic pressure required to effect a change in volume of the lung and thorax; it says nothing about gas flow. This pressure can be represented by the lateral distance between the static lung and chest wall compliance curves for the volume of interest (figure 3).

圖3.靜態(tài)呼吸壓力

肺和胸壁順應(yīng)性性曲線的斜率將隨不同的疾病狀態(tài)而變化。 肺順應(yīng)性曲線向左下移動(dòng)表示肺順應(yīng)性差，而胸壁順應(yīng)性曲線的右下偏移表示胸壁依從性惡化（圖4）。 肺順應(yīng)性的主要決定因素是表面活性物質(zhì)的存在和活性，肺的膠原和彈性蛋白成分則影響較小。胸壁順應(yīng)性的效果取決于骨性胸廓和腹部以及呼吸肌肉的活動(dòng)。 

The slope of both the pulmonary and chest wall compliance curves will shift with different disease states. A down-left shift of the pulmonary compliance curve represents poor pulmonary compliance while a down-right shift of the chest wall compliance curve depicts worsening chest wall compliance (figure 4). The main determinant of pulmonary compliance is the presence and activity of surfactant9; a less prominent influence is the collagen and elastin composition of the lungs.10 The effectors of chest wall compliance are the compliances of the bony thorax, and the abdomen as well as the activity of the muscles of respiration.

圖4.肺和胸壁順應(yīng)性性之間的關(guān)系

拔管和呼吸負(fù)荷

正壓降低了呼氣時(shí)氣道阻力，并有助于肺排空，推測(cè)通過(guò)像支架一樣開放了遠(yuǎn)端氣道。肺彈性回縮力的降低是阻塞性氣道疾病患者的常見情況，可造成在主動(dòng)呼氣期間從肺泡向氣道的壓力梯度減小。由此造成在更遠(yuǎn)側(cè)形成等壓點(diǎn)，在此點(diǎn)胸膜壓力超過(guò)氣道壓力，導(dǎo)致動(dòng)態(tài)氣道塌陷。這解釋了內(nèi)源性PEEP（Auto-PEEP）和氣體潴留的現(xiàn)象 ，這可能并發(fā)于拔管后期。 雖然動(dòng)態(tài)過(guò)渡通氣與氣體限閉?？苫ハ噢D(zhuǎn)換，但存在微妙的區(qū)別。 動(dòng)態(tài)的過(guò)渡通氣通常與肺彈性回縮力和肺氣腫有關(guān)，而氣體限閉甚至可發(fā)生在高彈性回縮力情況，如肺水腫和急性呼吸窘迫綜合征（ARDS）。 在過(guò)量肺水和ARDS的情況下發(fā)生的氣體限閉是高氣道阻力的結(jié)果，這可能是由于水腫，炎癥和下葉過(guò)高的閉合容積造成。

Positive pressure reduces expiratory airways resistance and facilitates emptying of the lung, putatively by stenting open distal airways. Decreased pulmonary elastic recoil, a common phenomenon in patients with obstructive airways disease, contributes to a decrement in the pressure gradient from the alveolus down the airway during active expiration. As a consequence, a more distal equal pressure point is generated in the airway at which the pleural pressure exceeds the airway pressure, leading to dynamic airway collapse.19,20 This physiology predicts the phenomena of auto-PEEP and air-trapping21,22 which may complicate the post-extubation period. While dynamic hyperinflation and air-trapping are often used interchangeably, there is a subtle distinction. Hyperinflation is classically associated with impaired pulmonary elastic recoil and emphysema, while air-trapping can occur in disease states typified even by high elastic recoil such as pulmonary edema and the acute respiratory distress syndrome (ARDS). The air-trapping that occurs in the setting of excess lung water and ARDS is the result of high airway resistance which may occur as a result of edema, inflammation and high closing volumes in the lower lobe.

隨著氣體限閉發(fā)展，肺內(nèi)壓力增加。 肺內(nèi)壓力是肺泡內(nèi)的壓力減去胸膜壓力; 這是決定肺容積的壓力差。 高肺容積將使肺實(shí)質(zhì)過(guò)渡牽拉，并延伸到其壓力 - 體積關(guān)系不良的部分。

As air-trapping progresses, the transpulmonary pressure increases. The transpulmonary pressure is the pressure within the alveolus minus the pleural pressure; it is the gradient which determines lung volume. High lung volume stretches the pulmonary parenchyma to a poorly compliant portion of its pressure-volume relationship.

總之，呼吸負(fù)荷由于氣道阻力高而增加，而高氣道阻力有利于應(yīng)對(duì)氣體限閉的低肺順應(yīng)性。 這些因素共同產(chǎn)生動(dòng)態(tài)環(huán)境，而心臟身處其中，暴露雙心室流出阻抗及心室壁張力的過(guò)度增加，這將在以下部分詳述。

In summary, respiratory load increases as a consequence of high airway resistance, while the high airway resistance favors low pulmonary compliance in response to air-trapping. Together these factors generate a dynamic environment whereby the heart is exposed to exaggerated biventricular outflow impedance and increases in ventricular wall tension as elaborated in the following sections.

......

以下因?yàn)槭痔?，關(guān)鍵段落不得不太監(jiān)了，哈哈......

Right ventricular outflow impedance

Arterial impedance may be modeled as the geometric summation of two biophysical properties: resistance and reactance. Vascular resistance tends to obey Poiseuille’s law, which states that resistance is inversely proportional to the radius of the vessel raised to the fourth power.32,33 Reactance is inversely related to both vascular compliance and cycle frequency; thus reactance helps account for vascular elasticity.34 While a single measure of right ventricular (RV) afterload is elusive,35,36 there is evidence that increases in pulmonary vascular resistance37, decreases in pulmonary arterial compliance38 and increases in transmural vascular pressure all may effectively increase RV afterload31, though the relative contributions of the resistive versus compliance components to total impedance may differ.29,36

The abnormally low pleural pressure that accompanies augmented respiratory load has differing effects on extra-alveolar versus intra-alveolar vessels. The extra-alveolar vessels (the large pulmonary arteries, veins and tributaries that lie outside of the alveolar wall) are directly exposed to pleural pressure. The bronchovascular bundle enters the lungs at the hila via an invagination of the visceral pleura. To the extent the transpulmonary pressure exceeds the vascular transmural pressure, the extraalveolar vessel will dilate during inspiration39 thereby facilitating a lower vascular resistance; this effect predominates at lung volumes less than FRC.40,41

The intra-alveolar vessels, in contradistinction, are exposed to alveolar pressure. West and colleagues proposed lung zones to describe the relationship between alveolar pressure and pulmonary vascular pressure.42 Zone II physiology occurs when alveolar pressure is greater than left atrial pressure. Zone II predominates when alveolar pressure is high, and/or left atrial pressure is low (e.g. dynamic hyperinflation with auto-PEEP). In this circumstance, the alveolar pressure becomes the pressure against which the right ventricle ejects.43

This relationship between air-trapping and right ventricular load was illustrated in a study by Harris and colleagues44. They found that exercise and voluntary hyperventilation in patients with obstructive airways disease led to increased pulmonary vascular resistance when compared to healthy controls and the degree to which this occurred was directly related to the severity of pulmonary disease.45,46

While the increased impedance to right ventricular outflow seems mostly mediated by increased vascular resistance as a consequence of increased lung volume, large negative deflections in thoracic pressure also appear to retard right ventricular ejection, though the underlying mechanisms are beyond the scope of this review.29,47,48

Ventricular interdependence

Transitioning from mechanical ventilation to spontaneous breathing can adversely affect the function of both ventricles and their interaction, through the phenomenon of ventricular interdependence. The filling status of one cardiac chamber can affect the filling properties of each of the other three chambers49, and filling one ventricle alters the pressure-volume relationship of the contralateral ventricle, in essence generating a dynamic diastolic dysfunction. The mechanism behind this effect is thought to be mediated via septal shift.50

Ventricular interdependence may be clinically relevant in acute exacerbations of obstructive airways disease31 or in any form of pulmonary hypertension.51 As right ventricular outflow impedance increases, a tendency to increase RV volume is established; this may diminish left ventricular stroke volume and raise the left ventricular end-diastolic pressure. To the extent that change in RV geometry impairs LV compliance and raises the left atrial pressure (which opposes RV ejection) the RV preload can become its own afterload.48

Interdependence is facilitated when the ventricular free walls or pericardium become stiff, and is mitigated when the ventricular septum becomes poorly compliant.52,53,54 Because the time-constants of the lower lobes tend to be higher,55 increased airways resistance promote gas-trapping preferentially near the heart. Butler and colleagues demonstrated that this can raise biventricular filling pressure and facilitate ventricular interdependence as the heart is squeezed by the increased volume of the lower lobes56; in effect, this physiology mirrors pericardial constriction.

The respiratory load imposed on a patient removed from positive pressure ventilation can thus raise right ventricular afterload and exaggerate right ventricular volume. Equally important is facilitation of right heart preload, also favored by removal of positive intrathoracic pressure. Spontaneous inspiration is marked by an increase in transdiaphragmatic pressure, that is, intra-abdominal pressure increases while intrathoracic pressure is diminished. Compression of the abdominal splanchnic vessels by abdominal pressurization augments the upstream pressure for venous return – the mean systemic filling pressure.57,58,59 Simultaneously, spontaneous ventilation decreases the downstream pressure for venous return – the right atrial pressure.60,61 Because the gradient for venous return is typically less than 10 mmHg, small changes in either the upstream or downstream pressure magnify total blood flow back to the right heart. Importantly, a high right atrial pressure at the onset of spontaneous ventilation establishes a great potential for venous return58,62 and this will heighten ventricular interdependence.

Respiratory load and the left ventricle

Reducing the pressure surrounding the left ventricle and thoracic aorta relative to the extrathoracic compartment impairs the egress of blood from the thorax.27,29,63 This physiology is typically explained using the modified law of LaPlace28, that is, as the ambient pressure falls relative to the intraluminal pressure of the left ventricle, the transmural wall stress is increased; this retards ventricular systole. An exaggerated fall in intrathoracic pressure impairs left ventricular output by both diastolic (e.g. ventricular interdependence) and systolic (e.g. augmentation of afterload) events.64,65,66,67 When the greatest drop in pleural pressure coincides with ventricular diastole, the diminution in left ventricular stroke volume is primarily a consequence of the right heart impairing left heart compliance. By contrast, a plunge in intra-thoracic pressure which occurs during ventricular systole impairs left ventricular stroke volume as a result of high impedance to flow.

Enhanced pulmonary venous return accompanying each inspiratory rise in lung volume may further compound the situation. As the transpulmonary pressure is rises above functional residual capacity, the capacitance of the alveolar blood vessels is diminished. This tends to raise the pressure head for pulmonary venous return; in effect the left heart is bolused which each inspiration. In an analogous physiology to the abdomen’s68, the fraction of West Zone III physiology determines the degree of pulmonary venous return. In a lung that is relatively fluid overloaded (i.e., with a high West Zone III fraction), the inspiratory increase in pulmonary venous return will be accordingly large.

Thus, an inspiratory drop in intrathoracic pressure leads to both diastolic and systolic events that impair left ventricular stroke volume. In conjunction with enhanced pulmonary venous return as lung volume increases, a milieu is created that favors increases in the left ventricular filling pressure and the development of pulmonary edema.

Excess cardiorespiratory load and the formation of pulmonary edema

The aforementioned pathophysiological pathways ultimately result in high left ventricular filling pressure. This effect will diminish the gradient for pulmonary venous return and favor excess lung water. Historically, the investigation into the pathogenesis of pulmonary congestion and edema concentrated upon isolated stages of fluid overload.69,70 Both decreased pulmonary compliance, increased airway resistance and therefore high breathing work have been noted in each of these stages. The stages of increased lung water, in order of sequence, have been considered to be: pulmonary vascular engorgement, bronchovascular interstitial edema, alveolar interstitial edema followed by frank alveolar flooding.70

Pulmonary vascular engorgement, the first stage of excess lung water is clinically marked by ‘cephalization’ of the pulmonary vasculature on a simple chest radiograph.71 Even during this early stage there is an associated drop in pulmonary compliance in humans, though this effect tends to be minimal.72 The mechanism of impaired compliance is felt to be the result of auto-regulatory active vascular tension according to the myogenic theory of blood flow. The greatest decrement in pulmonary compliance occurs during the later stages of pulmonary edema, especially with frank alveolar flooding.73 Along with alveolar and airway edema, there is an accumulation of intraluminal bubble froth, which reduces pulmonary compliance by decreasing alveolar radius and interfering with surfactant function.74

Respiratory load is increased not only by impaired pulmonary compliance during states of excess lung water. Airway resistance is increased with pulmonary vascular engorgement and edema.73,74 Animal models75 propose that in the early stages of increased lung water, the vagus nerve mediates a reflex increase in airway resistance; bronchovascular interstitial edema progresses and physically impinges upon the airways.76,77,78 With frank alveolar edema, bubble froth plugs the small airways and leads to the greatest increase in resistance.74

Conclusion

圖5中的模式說(shuō)明了在本文中所述的“肺阻塞”和“肺充血”病理生理學(xué)條件下呼吸系統(tǒng)和心血管系統(tǒng)之間的可能相互作用。 首先是右心室流出干擾可促進(jìn)左心室功能障礙，而左心室功能受損和肺水過(guò)多可促進(jìn)和惡化右心功能。 盡管不是每個(gè)患者在機(jī)械通氣撤除時(shí)這些機(jī)制都發(fā)揮作用，但該圖突出了呼吸和心血管病理生理學(xué)之間的相互關(guān)系。 除了肺阻力和胸部順應(yīng)性之外，當(dāng)考慮患者解除機(jī)械通氣時(shí)，應(yīng)考慮并優(yōu)化雙心室前負(fù)荷和后負(fù)荷。 對(duì)這些病理生理機(jī)制的重視，特別是慢性心肺疾病患者，可能有助于防止機(jī)械通氣解除后的心肺衰竭，——一個(gè)少見但潛在災(zāi)難性的情況。

The schema in figure 5 illustrates the possible interactions between the respiratory and cardiovascular systems in conditions of both “obstructive-lung” and “congested-lung” pathophysiology as described in this review. Primary perturbations in right ventricular outflow can facilitate left ventricular dysfunction, whereas states of impaired left ventricular function and excess lung water can facilitate and worsen right heart function. Although not each of these mechanisms is at play in every patient relieved from mechanical ventilation, the diagram does highlight the interrelationship between respiratory and cardiovascular pathophysiology. In addition to pulmonary resistance and thoracic compliance, biventricular preload and afterload should be contemplated and optimized when considering a patient for liberation from mechanical ventilation. Respect for these pathophysiologic mechanisms, especially in patients with chronic cardiopulmonary illness, may help prevent cardiorespiratory collapse following liberation from mechanical ventilation, an infrequent but potentially catastrophic scenario.

圖5. “肺阻塞”和“肺充血”狀態(tài)下潛在的心肺系統(tǒng)相互作用