Alvarado Andrea C, Pinsky Michael R
Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
Front Physiol. 2023 Aug 8;14:1237741. doi: 10.3389/fphys.2023.1237741. eCollection 2023.
The primary impact of ventilation and ventilatory efforts on left ventricular (LV) function in left ventricular dysfunction relate to how changes in intrathoracic pressure (ITP) alter the pressure gradients for venous return into the chest and LV ejection out of the chest. Spontaneous inspiratory efforts by decreasing ITP increase both of these pressure gradients increasing venous blood flow and impeding LV ejection resulting in increased intrathoracic blood volume. In severe heart failure states when lung compliance is reduced, or airway resistance is increased these negative swings in ITP can be exacerbated leading to LV failure and acute cardiogenic pulmonary edema. By merely reversing these negative swings in ITP by the use of non-invasive continuous positive airway pressure (CPAP), these profoundly detrimental forces can be immediately reversed, and cardiovascular stability can be restored in moments. This forms the clinical rationale for the immediate use of CPAP for the treatment of acute cardiogenic pulmonary edema. Increasing ITP during positive pressure ventilation decreases the pressure gradients for venous return and LV ejection decreasing intrathoracic blood volume. In a hypovolemic patient even with LV dysfunction this can result in hypotension due to inadequate LV preload. Minor increases in ITP as occur using pressure-limited positive-pressure ventilation primarily reverse the increased LV afterload of negative swings in ITP and if fluid overload was already present, minimally alter cardiac output. The effect of changes in lung volume on LV function are related primarily to its effects on right ventricular (RV) function through changes in pulmonary vascular resistance and overdistention (hyperinflation). In acute lung injury with alveolar collapse, positive pressure ventilation may reduce pulmonary vascular resistance if alveolar recruitment predominates. Hyperinflation, however, impedes diastolic filling while simultaneously increasing pulmonary vascular resistance. Thus, increasing lung volume can reduce RV afterload by reversing hypoxic pulmonary vasoconstriction or increase afterload by overdistention. Hyperinflation can also impede RV filling. All of these processes can be readily identified at the bedside using echocardiography.
通气及通气努力对左心室功能不全患者左心室（LV）功能的主要影响，涉及胸内压（ITP）变化如何改变静脉血回流至胸部以及左心室射血至胸部的压力梯度。自主吸气努力通过降低ITP增加这两个压力梯度，增加静脉血流量并阻碍左心室射血，导致胸内血容量增加。在严重心力衰竭状态下，当肺顺应性降低或气道阻力增加时，ITP的这些负向波动会加剧，导致左心室衰竭和急性心源性肺水肿。通过使用无创持续气道正压通气（CPAP）仅仅逆转这些ITP的负向波动，这些严重有害的力量可立即被逆转，心血管稳定性可在瞬间恢复。这构成了立即使用CPAP治疗急性心源性肺水肿的临床理论依据。正压通气期间增加ITP会降低静脉血回流和左心室射血的压力梯度，减少胸内血容量。在低血容量患者中，即使存在左心室功能不全，这也可能因左心室前负荷不足而导致低血压。使用压力限制正压通气时出现的ITP轻微增加，主要是逆转ITP负向波动导致的左心室后负荷增加，如果已经存在液体过载，则对心输出量的影响最小。肺容积变化对左心室功能的影响主要通过肺血管阻力和过度扩张（肺过度充气）的变化对右心室（RV）功能的影响来体现。在伴有肺泡萎陷的急性肺损伤中，如果肺泡复张占主导，正压通气可能会降低肺血管阻力。然而，肺过度充气会阻碍舒张期充盈，同时增加肺血管阻力。因此，增加肺容积可通过逆转低氧性肺血管收缩来降低右心室后负荷，或因过度扩张而增加后负荷。肺过度充气还会阻碍右心室充盈。所有这些过程都可以在床边通过超声心动图轻松识别。
