Negative intrathoracic pressure decreases independently left ventricular filling and emptying.

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.