Peters J, Fraser C, Stuart R S, Baumgartner W, Robotham J L
Pulmonary Anesthesia Laboratory, Francis Scott Key Medical Center, Johns Hopkins University Medical Institutions, Baltimore, Maryland 21205.
Am J Physiol. 1989 Jul;257(1 Pt 2):H120-31. doi: 10.1152/ajpheart.1989.257.1.H120.
The mechanism for the fall in left ventricular (LV) stroke volume with normal and obstructed inspiration is controversial with changes proposed in LV preload and afterload. During respiration extending over several cardiac cycles, changes in both LV filling and emptying could occur, rendering demonstration of any responsible mechanism difficult. To evaluate the independent effects of negative intrathoracic pressure (NITP) on LV filling and emptying, we have analyzed the effects of NITP confined to either diastole or systole using electrocardiogram (ECG)-triggered phrenic nerve stimulation in six anesthetized closed-chest dogs. Lung volume was either maintained by completely obstructing the airway or allowed to increase during NITP. With diastolic NITP and the airway obstructed during phrenic nerve stimulation, LV filling volume (integrated mitral flow) significantly decreased (-37 +/- 6.1% SE) associated with increases in LV and right atrial filling pressures at end diastole relative to both atmospheric and esophageal pressures. Right atrial pressure relative to either atmospheric or esophageal pressure increased significantly more than left atrial pressure. The ensuing LV stroke volume (integrated ascending aortic flow) decreased significantly (-30.8 +/- 5.9%). With NITP confined to systole and at constant LV preload, LV stroke volume also decreased (-12.9 +/- 2.5%) associated with an increase in LV systolic pressure relative to esophageal pressure. Similar significant changes were observed despite a smaller fall in esophageal pressure when lung volume was allowed to increase during either diastolic or systolic NITP. We conclude that 1) NITP confined to diastole decreases LV filling and the ensuing LV stroke volume, most likely by ventricular interdependence; 2) NITP confined to systole also decreases LV stroke volume, presumptively by imposing an increased afterload on the LV; 3) both diastolic and systolic mechanisms should contribute to a decreased LV stroke volume during normal and obstructed inspiration; and 4) if the effects of intrathoracic pressure changes were to extend over several cardiac cycles, mechanisms exist to account for either increases or decreases in LV volumes.
正常吸气和阻塞性吸气时左心室（LV）每搏输出量下降的机制存在争议，有人提出这与左心室前负荷和后负荷的变化有关。在跨越多个心动周期的呼吸过程中，左心室充盈和排空都会发生变化，这使得证明任何相关机制都很困难。为了评估胸内负压（NITP）对左心室充盈和排空的独立影响，我们在六只麻醉的开胸犬中使用心电图（ECG）触发的膈神经刺激分析了局限于舒张期或收缩期的胸内负压的影响。在膈神经刺激期间，通过完全阻塞气道来维持肺容积，或者在胸内负压作用下允许肺容积增加。在膈神经刺激期间，当气道阻塞且存在舒张期胸内负压时，左心室充盈容积（二尖瓣血流积分）显著下降（-37±6.1%，标准误），与舒张末期相对于大气压和食管压力的左心室和右心房充盈压升高有关。相对于大气压或食管压力，右心房压力升高明显超过左心房压力。随后的左心室每搏输出量（升主动脉血流积分）显著下降（-30.8±5.9%）。当胸内负压局限于收缩期且左心室前负荷恒定时，左心室每搏输出量也下降（-12.9±2.5%），与相对于食管压力的左心室收缩压升高有关。当在舒张期或收缩期胸内负压作用下允许肺容积增加时，尽管食管压力下降幅度较小，但仍观察到类似的显著变化。我们得出以下结论：1）局限于舒张期的胸内负压会降低左心室充盈及随后的左心室每搏输出量，最可能是通过心室相互依赖作用；2）局限于收缩期的胸内负压也会降低左心室每搏输出量，推测是通过增加左心室的后负荷；3）舒张期和收缩期机制都应导致正常吸气和阻塞性吸气时左心室每搏输出量下降；4）如果胸内压变化的影响延伸至多个心动周期，则存在可解释左心室容积增加或减少的机制。
Zotero 插件