Cardiovascular regulation
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
