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Cardiopulmonary physiology: why the heart and lungs are inextricably linked

机译:心肺生理学:为什么心脏和肺部有着千丝万缕的联系

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Because the heart and lungs are confined within the thoracic cavity, understanding their interactions is integral for studying each system. Such interactions include changes in external constraint to the heart, blood volume redistribution (venous return), direct ventricular interaction (DVI), and left ventricular (LV) afterload. During mechanical ventilation, these interactions can be amplified and result in reduced cardiac output. For example, increased intrathoracic pressure associated with mechanical ventilation can increase external constraint and limit ventricular diastolic filling and, therefore, output. Similarly, high intrathoracic pressures can alter blood volume distribution and limit diastolic filling of both ventricles while concomitantly increasing pulmonary vascular resistance, leading to increased DVI, which may further limit LV filling. While LV afterload is generally considered to decrease with increased intrathoracic pressure, the question arises if the reduced LV afterload is primarily a consequence of a reduced LV preload. A thorough understanding of the interaction between the heart and lungs can be complicated but is essential for clinicians and health science students alike. In this teaching review, we have attempted to highlight the present understanding of certain salient aspects of cardiopulmonary physiology and pathophysiology, as well as provide a resource for multidisciplined health science educators and students.
机译:由于心脏和肺部被限制在胸腔内,因此了解它们的相互作用对于研究每个系统都是必不可少的。此类相互作用包括心脏外部约束的变化,血容量的重新分配(静脉回流),直接的心室相互作用(DVI)和左心室(LV)后负荷。在机械通气期间,这些相互作用会被放大并导致心输出量降低。例如,与机械通气相关的胸腔内压力升高会增加外部约束并限制心室舒张期充盈,从而限制输出。同样,高胸腔内压力会改变血容量分布并限制两个心室的舒张期充盈,同时伴随增加肺血管阻力,导致DVI升高,这可能进一步限制LV充盈。虽然通常认为LV后负荷会随着胸腔内压力的增加而降低,但问题是,如果LV后负荷的降低主要是由于LV预负荷降低所致。对心脏和肺之间相互作用的透彻理解可能很复杂,但对于临床医生和健康科学专业的学生而言都是必不可少的。在本教学评论中,我们试图强调对心肺生理学和病理生理学某些显着方面的当前理解,并为多学科的健康科学教育者和学生提供资源。

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