This is a lecture we did on Respiratory for my medic students. It is gonna be a multi-part series and I hope you like it!

CORRECTION: (Thanks to the point from my student Post, awesome job man!!!!)
The part where preload is addressed is incorrect. During normal negative pressure ventilation, preload actually increases as opposed to PPV where preload will decrease. LVEDP will decrease during negative pressure ventilation but the net effect is an overall decrease.

Pressures in the right atrium and thoracic vena cava are very dependent on intrapleural pressure (Ppl ), which is the pressure within the thoracic space between the organs (lungs, heart, vena cava) and the chest wall. During inspiration, the chest wall expands and the diaphragm descends (see animated figure). This makes the Ppl become more negative, which leads to expansion of the lungs, cardiac chambers (right atrium [RA] and right ventricle [RV]), and the thoracic superior and inferior vena cava (SVC and IVC, respectively). This expansion causes the intravascular and intracardiac pressures (e.g., right atrial pressure) to fall. Because the pressure inside the cardiac chambers falls less than the Ppl, the transmural pressure (pressure inside the heart chamber minus the Ppl) increases, which leads to cardiac chamber expansion and an increase in cardiac preload and stroke volume through the Frank-Starling mechanism. Furthermore, as right atrial pressure falls during inspiration, the pressure gradient for venous return to the right ventricle increases. During expiration, the opposite occurs although the dynamics are such that the net effect of respiration is that increasing the rate and depth of ventilation facilitates venous return and ventricular stroke volume.

The left side of the heart responds differently to the respiratory cycle. During inspiration, expansion of the lungs and pulmonary tissues causes pulmonary blood volume to increase, which transiently decreases the flow of blood from the lungs to the left atrium. Therefore, left ventricular filling actually decreases during inspiration. In contrast, during expiration, lung deflation causes flow to increase from the lungs to the left atrium, which increases left ventricular filling. The net effect of increased rate and depth of respiration, however, is an increase in left ventricular stroke volume and cardiac output.