心肺交互作用(simplified)

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

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↑
Whittenberger JL, et al. J Appl Physiol 1960;15:878–82.
Intensive Care Med (2009) 35:45–54

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
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):


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).


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

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 PA>Pa
受肺泡压力影响区域血管彻底塌陷
▪ 血流消失
▪ 死腔通气

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 Nhomakorabea
全肺PA=0±2 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



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

Zone 1: PA > Pa > Pv Zone 2: Pa > PA > Pv Zone 3: Pa > Pv > PA

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: 713–24.
CCM.2009



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.