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a] the intrathoracic pressure variations
b] the LV-preload [11]
c] the vasomotor system
All three are indirectly affected by the respiratory activity, either spontaneous or artificial. The influence of a] аnd b] takes place at the respiratory frequency. The influence of c] acts slower because of the time constant of the neural pathway involved [sympathetic nervous system]. The heartrate influences the LV-preload indirectly, regulating the ventricle filling time.

In more detail the relations can be explained as follows:

• Part of the intrathoracic pressure variations is transduced to the adjacent tissues аnd organs. The pressure variations decrease when the point of measurement is further from the lungs. Due to the compliant nature of many parts of the body, the pressure has been reduced gradually due to an increase of the surrounding volume. In the thoracic region, however, many of the pressure variations still exist аnd are superimposed on all organs, including the cardiovascular system. This leads directly to a variation in the blood pressure signal level. In the central venous pressure this pressure variation can also be recognised. The pressure transduction is almost instantaneous, so in relation to the extension of the lungs no significant delay will be present. If the inspiration is spontaneous, a pressure decrease will take place; in case of artificial ventilation with positive pressure ventilation, a pressure increase will take place.
• The second influence on the blood pressure is due to the change in venous return when the intrathoracic pressure changes. During inspiration the intrathoracic pressure decreases, increasing the venous return. This higher RA-preload leads to a higher blood flow through the lungs, a higher LV-preload аnd thus a higher cardiac output. Due to the increased cardiac output the blood pressure will increase. The whole process will take about 2 heartbeats. Normally there are two stabilising counter-influences on the increase of venous return during inspiration. The first one consists of the increase of the heartrate, causing the higher RV volume to be pumped out earlier [12]. The second one consists of the squeezing out of blood from the lungs during expiration. If expiration follows one heartbeat after inspiration, the LV-preload is being increased extra, by delay due to the increased venous return, аnd due to the squeezing out of blood from the lungs. So, depending on the respiratory frequency different increasing аnd decreasing effects on blood pressure might be observed. Changes in heartrate will affect the LV-preload because of variations in the ventricle filling time. Apart from the mechanism described above the heartrate will variate due to the so-called Respiratory Sinus Arrythmia [RSA]: parallel to phrenic nerve activity [respiration] the parasympathetic irradiation of the SA-node is being inhibited, leading to an increase in heart rate, respiratory sinus arrhythmia, RSA, t = 0.1 s after start of inspiration]. It still is a matter of debate whether this mechanism exists, and, if so, whether it primarily causes RSA. Another contributor to the RSA is the baroreceptor reflex: the aortic arch аnd stretch receptors in the carotid sini reflect pressure changes through vagal as well as sympathetic pathways; an increase in pressure results in a higher vagal activity to the sinus node, prolonging the current heart interval. The sympathetic influence is opposite аnd slower [scale of seconds] аnd only plays a role below the respiratory frequency.
• Thirdly, the blood pressure is influenced by the vasomotor system. This system regulates the peripheral resistance аnd muscle tone of the vessels. The respiration modulates the vasomotor system sympathetically. The low-pass character of the sympathetic activity only leads to an averaged respiratory influence on the vasomotor system. The averaged variations that result on blood pressure are called Breath Amplitude Sinus Arrhythmia [BASA]. This influence becomes important at the respiratory frequency itself when it drops to approximately 0.2 Hz or less [within the bandwidth of the sympathetic nervous system], which is very unlikely in neonates. A back-regulation also exists from the blood pressure to the vasomotor system. It is also sympathetically mediated. We conclude that due to the integrative effect only the average respiration frequency influences blood pressure by variation of the vasomotor characteristics. An influence on blood pressure in neonates can thus be expected due to breath amplitude variations at the lower frequencies. The closed circuit 13,15 may result in oscillatory changes, the so-called Mayer waves .