The right ventricle: interaction with the pulmonary circulation.
The right ventricle: interaction with the pulmonary circulation.
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右心室：与肺循环的相互作用。
DOI：
10.1186/s13054-016-1440-0
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发表时间：
2016-09-10
期刊：
影响因子：
--
通讯作者：
Pinsky MR
中科院分区：
文献类型：
--
作者：
Pinsky MR
右心室(RV)的主要作用是将它每搏动接收的所有血液输送到肺循环中，而不会导致右心房压力上升。在不妨碍左心室(LV)充盈的情况下，心输出量对增加的代谢需求的反应被优化。由于心输出量是身体代谢需求的函数，在应激和运动状态下，流向RV的流量可能会有很大的变化。此外，瞬时静脉回流对于恒定的心输出量变化很大，因为呼吸机的努力改变了静脉回流的动态压力梯度。正常情况下，血流变化很小，对肺动脉压的影响很小。同样，右室充盈通常发生在右房压力轻微增加的情况下。当肺血管储备受损时，右室射血也可能受损，增加右房压力，限制最大心输出量。右室流出阻力的急剧增加，如急性肺栓塞可能发生的，将导致急性右室扩张，并通过心室的相互依赖性，显著降低左室舒张期顺应性，迅速螺旋式上升为急性心源性休克和死亡。治疗方法包括逆转肺动脉高压的病因，将高于肺动脉压的平均动脉压维持在最大右室冠脉血流量。慢性肺动脉高压导致右室进行性肥大，使右室的收缩能力与增加的肺动脉弹性相匹配。一旦完全发展，右室肥厚与右房压力持续增加、左室充盈受损和运动耐量降低有关。治疗的重点是有选择地降低肺血管舒张性张力和利尿剂的药物治疗，以最大限度地减少RV过度扩张。由于大多数形式的肺动脉高压的不可逆性，当由于右室扩张、进行性肺血管闭塞或两者兼而有之，当肺动脉弹性大大超过右室收缩弹性的适应性增加时，就会发生终末期肺心病。如果合并心源性休克，只有通过人工脑室支持或肺移植才能有效治疗。了解房车是如何适应这些压力的，它的标志和治疗方案将极大地提高床边临床医生诊断和治疗房车功能障碍的能力。
The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to rise. To the extent that it also does not impede left ventricular (LV) filling, cardiac output responsiveness to increased metabolic demand is optimized. Since cardiac output is a function of metabolic demand of the body, during stress and exercise states the flow to the RV can vary widely. Also, instantaneous venous return varies widely for a constant cardiac output as ventilatory efforts alter the dynamic pressure gradient for venous return. Normally, blood flow varies with minimal changes in pulmonary arterial pressure. Similarly, RV filling normally occurs with minimal increases in right atrial pressure. When pulmonary vascular reserve is compromised RV ejection may also be compromised, increasing right atrial pressure and limiting maximal cardiac output. Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to acute cardiogenic shock and death. Treatments include reversing the causes of pulmonary hypertension and sustaining mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary hypertension induces progressive RV hypertrophy to match RV contractility to the increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is associated with a sustained increase in right atrial pressure, impaired LV filling, and decreased exercise tolerance. Treatment focuses on pharmacologic therapies to selectively reduce pulmonary vasomotor tone and diuretics to minimize excessive RV dilation. Owning to the irreversible nature of most forms of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds the adaptive increase in RV systolic elastance, due to RV dilation, progressive pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If associated with cardiogenic shock, it can effectively be treated only by artificial ventricular support or lung transplantation. Knowing how the RV adapts to these stresses, its sign posts, and treatment options will greatly improve the bedside clinician’s ability to diagnose and treat RV dysfunction.
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影响因子：
9.6
作者：
JARDIN, F;GUERET, P;BOURDARIAS, JP
通讯作者：
BOURDARIAS, JP
DOI：
10.1016/j.jtcvs.2009.11.020
发表时间：
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影响因子：
9.6
作者：
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