Pulmonary ventilation is commonly referred to as breathing. It is the process of air flowing into the lungs during inspiration inhalation and out of the lungs during expiration exhalation.
Air flows because of pressure differences between the atmosphere and the gases inside the lungs. Air, like other gases, flows from a region with higher pressure to a region with lower pressure. Muscular breathing movements and recoil of elastic tissues create the changes in pressure that result in ventilation. Pulmonary ventilation involves three different pressures:.
During muscle relaxation, the proximal valves open and blood flows into and fills the venous segment. Initially during relaxation, the distal valves close, but then they open as the volume of blood and pressure increases in the venous segment. The net effect is that the cycle of compression and relaxation propels the blood in the direction of the heart. Venous valves prevent the blood from flowing backwards, thereby permitting unidirectional flow that enhances venous return.
When a person is standing, postural muscles in the legs alternately contract and relax to keep the body in balance. This muscle activity promotes venous return and helps to maintain central venous pressure and venous return, and to lower venous and capillary pressures in the feet and lower limbs.
Respiratory activity influences venous return to the heart. Briefly, increasing the rate and depth of respiration promotes venous return and therefore enhances cardiac output. Non-typical respiratory activity such as being on positive pressure ventilation or doing a forced expiration against a closed glottis Valsalva maneuver impedes and therefore reduces venous return and cardiac output.
Respiratory activity affects venous return through changes in right atrial pressure, which is an important component of the pressure gradient for venous return. Increasing right atrial pressure impedes venous return, while lowering this pressure facilitates venous return. Animal studies indicate that with airway obstruction, for the first beat or two of inspiration the primary effect on the LV is a reduction in stroke volume related to a decrease in preload, and afterload, if anything, decreases.
In fact, afterload only increases during early expiration when stroke volume increases. When obstructive and central apnoeas are paired for duration and blood-gas alterations, there are increases in pulmonary blood volume with central apnoeas and in RV volume with obstructive apnoeas, consistent with the postulation that the primary effect of obstructive apnoeas is on venous return.
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