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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 .

The task of the cardiovascular system is proper regulation of the blood flow to all organs аnd tissues. The required blood flow depends on necessitate for oxygen & nutrition of the particular organs. During physical stress, example, the supplied blood of the active muscles will rapidly increase. In that condition the heart will have to pump through more blood per minute, аnd a constriction of the arterioles in the peripheral tissues will takes place to raise the peripheral resistance аnd maintain the level of the arterial blood pressure. In the regulation of the blood flow a large number of neural, chemical аnd humoral factors is involved. Apart from these, the cardiovascular system is influenced by the respiratory activity. On one hand it consists of a direct influence of the vasomotor centre by the respiratory centre, the other by intrathoracic pressure fluctuations cause by respiration.

Inventory of interactions involving the cardiovascular system

Blood pressure variations are caused by several different effects. These effects can be subdivided in direct pressure components, neural components аnd circulatory components. A scheme of the cardiovascular interactions known in adults. First, we will point out the relevant information аnd assumptions about each of the relations. To what extent the interactions hold in neonates is not yet clear.
Qualitatively, they may apply as well, but it is likely that they will quantitatively differ
from the adult interactions.

1.> Sympathetic vasomotor actions, the central origin, modulated by central respiratory activity. Resulting to the influences peripheral resistance, of the muscle tone of other vessels.
Increase sympathetic tone ---> constriction of the vessels
t = 6 - 10 sec

2.> Sympathetic activity, central origin, modulated by central respiratory effort, efferent to the SA-node.
Increase sympathetic tone ---> increase in heart-rate.
t = 6 - 10 sec
In adults the respiratory influence on heart-rate exists at low respiratory frequencies [approximately < 0.2 Hz]

3.> Parasympathetic activity [vagal], central origin, modulated by central respiratory effort, efferent to the SA-node.
Increase parasympathetic tone ---> decrease in heart-rate
t = 0.2 - 0.4 sec [influence posible sustain]

4.> Respiratory centre trigger the intercostals muscles аnd diaphragm muscles to elevate the breast & thus induces intrathoracal to cause pressure changes. For spontaneous ventilation a negative intrathoracic pressure resulting of air inflowr, a positive pressure resulting in outflow. For artificial ventilation distension of the lungs is normally caused by the positive pressure of the machine instead of negative pressure.
impulsive inspiration ---> decrease pressure
synthetic insufflations ---> increase pressure
t = 0.05 s or less [direct]

5.> Part of the pressure under 4 is transmitted to the arterial system, especially in the thorax. This
influence is still present in the arterial wave form in the periphery. The direct component of
intrathoracic pressure change has an almost instantaneous influence on blood pressure. A part of the intrathoracic pressure is mediated to the arterial system. This influence may depend on the actual part of the heart cycle. A difference in mediation of the pressure depending on the compliance of the artery is likely. Consequently it will differ between systolic
phase аnd diastolic phase.
Increase thoracic pressure ---> increase BP
t = 0.05 sec / less

6.> Extension of stretch receptors in the lungs inhibits inspiratory effort. Vagally mediated аnd called
Hering-Breuer reflex .
During shallow respiration the frequency is not affected. During inspiration with a large tidal
volume, the frequency may be decreased.
t = 0.1 sec

7.> Pressure fluctuations in the thorax modulate the venous return.
Spontaneous inspiration ---> decrease in intrathoracic pressure ---> increase in venous return
t = 0.4 sec

8.> Lung & thoracic wall extend receptors vagally modulate heart-rate. It is assumed this only gives a
marginal contribution.
Extension of receptors ---> increase heart-rate
t = 0.1 sec

9.> Change in venous preload causes a change in right ventricular [RV] output to the lungs.
preload increase at the Right atrium [RA] ---> increase RV output ---> preload Increase the heart-beat
at the left ventricular [LV]

10.> Squeezing out the lung circulation on expiration yields an increase in LV preload
t = 0.1 s from expriation

11.> LV preload changes cause a change in cardiac output [given a constant heartbeat].
Increase in LV preload ---> increase in cardiac output аnd contractility ---> increase in BP [if
vasomotor state remains unchanged].
from venous return increase: t = 0.4 sec
from squeezing out of the lungs: t = 0.1 sec

12.> Bainbridge reflex, vitally mediated
Increased filling of the atria ---> increase in heartrate

13.> Sympathetic influence on the vasomotor system [or the sympathico-vagal balance].
Sympathetic increase ---> constriction of the vessels
t=≈6 sec

14.> Baroreceptor reflex; extend receptors in the aortic arch аnd carotids
Increase in BP ---> decrease in heartrate
t = 0.3 sec [vagally]

15.> Vasomotor state determines the resistance аnd compliance of the vascular system [sympathetic];
strong influence on BP.
Increased symp. irradiation ---> increase of BP [constriction of the vessels]
t>6 sec
t > ≈ 6 sec [sympathetically]

16.> The heartrate determines the filling time of the atria.
Heartrate increase ---> shorter filling time ---> decrease in RA preload. coming heartbeat

The nervous system can be divided in the central nervous system [CNS] аnd the peripheral nervous system. The central nervous system consists of the brain, the brainstem аnd the spinal cord. The peripheral nervous system consists of afferent nerves, which transmit information from the receptors to the CNS, аnd efferent nerves, which transmit information from the CNS to smooth muscles, the heart muscle, skeletal muscles аnd glands. The nervous sytem can also be divided in the voluntary аnd involuntary nervous sytem. The voluntary system takes care of the interaction of the body with the environment. The involuntary nervous system, also called the autonomic nervous system is involved in the innervation of the heart, the glands аnd the blood vessels: in short, the visceral system. It is involved in the maintenance of general homeostasis. The autonomic nervous sytem consists of 2 different working parts; 1.) The parasympathetic аnd the sympathetic nervous system. Nearly all innervated organs are innervated by both systems. The peripheral blood vessels аnd the adrenal аnd sweat glands, however, are only innervated by the sympathetic system.

Parasympathetic аnd sympathetic nervous system

The parasympathetic nerves are located in the brain stem аnd in the sacral part of the vertebral column, also called the craniosacral part. An important parasympathetic nerve, the nervus vagus, leaves from the brain stem. It innervates, among others, the heart, the lungs, аnd the stomach. The nerves from the sacral part drive the bladder, the genitals, аnd lower intestines.


The sympathetic nerves are situated in the thoracolumbar part of the autonomic nervous system. The nerves for head аnd neck start from the upper thoracal segments. The nerves in the thoracal as well as the lumbal part innervate the organs in the breast аnd abdomen. Table I illustrates the influence of parasympathetic resp. sympathetic system on some organs. An action potential is transferred from one
nerve to another nerve through a synapse. Such a transfer takes place in clusters of nervous cells, ganglia. There is a clear difference between the sympathetic аnd the parasympathetic nervous system. In contrast to the sympathetic nervous system, in the parasympathetic nervous system the ganglia are located close to the effector organs. The sympathetic part they located close to the spinal cord. The sympathetic part forms a network, in contrast to the parasympathetic that goes directly to the organs to be innervated. The parasympathetic system works within several tenth of a second, while the sympathetic system works only after several seconds.

Effects of symphatic аnd parasymphatic nerves on various organs

Organ                                               sympathetic effect                      parasympathetic effect
Heart                                                       acceleration                                            retardation
Arterioles                                                 constriction                                        generally no effect
Bronchi                                                      dilatation                                              constriction
Iris pupil                                                     dilatation                                           pupil narrowing
Bladder                                                      relaxation                                              contraction