Pressure, Flow and Resistance. Good to watch! Diagramm shows that there is no autocontrol out of range that you have specified. Vessels rich their limits.

https://www.youtube.com/watch?v=rkJA8oUO27Q

thanks for the answer,

but  if we have an hypertension, so we can reach levels higher than 160 mmHg on systolic pic, how the vessel will support the difference of pressure?

also, in the presence of an aneurysm, generally this anomaly will induce high pressure, so how the vessel wall will be considered, as a rigid wall or it can only go to dilatation ?

Thank you very much 

I did apply some techniques to control baro reflex  receptors via CN9 and CN10. 

Thank you for your answer.

so will ask you the same questions about the behavior of the bood vessel with high pressure?

thank you again 

best regards 

Dear Djalal,

Nice question! Ali is right to point out that much remains unknown about the regulation of these processes.

It is wonderful that we can sleep, work and sport and our cerebral blood flow (CBF) is still about 50 ml/100g/min. Even a handstand made us not really sick. J

Surgery, anesthesia and critical care are special circumstances, which was not directly figured out by nature …

In the “classical model” CVR, CPP and CBF are commonly defined by the law of Darcy as the quotient between the driving blood pressure and flow. This model has limitations, because it assumes that flow or velocity only reaches zero when the driving pressure is zero, which is unlikely. Patients without cerebrovascular disease are expected to have a normal ICP between 7-15 mmHg in supine position. Thus, the main determinant of the driving pressure would be the MAP. However, measures of MAP do not directly reflect the CPP because the CPP is modified by several factors. When calculating the CPP, the MAP has been used as effective upstream pressure (EUP) and the intracranial pressure (ICP) as effective downstream pressure (EDP) of the cerebral circulation, because of a Starling resistor phenomenon located at the level of cerebral veins.

 Studies of other organs as well as the brain have shown, that the EDP is more determined by a critical closing pressure located at arteriolar level. The concept of “critical closing pressure (CCP)” was considered by Burton and addressed for the cerebral circulation by Greenfield and Tindall and later by Dewey and Early, These studies verified the theory of Permutt and Riley showing that two forces, the extramural pressure (ICP in the case of the brain) and arteriolar wall tension, cause the CCP. Arteriolar wall tension arises from a combination of the stretched elastic components of the vessel wall and active contraction of vascular smooth muscle. Thus, the driving pressure for the flow through arterioles is, under many conditions, not the difference between arterial (inflow) pressure and venous (outflow) pressure, but rather the difference between arterial pressure and CCP.

It has been proven that in vivo pressure/flow relationships are straight lines for many vascular beds and even for the cerebral vessels. The intercept of the pressure/flow plot (zero flow pressure, the pressure when flow ceases), estimated by linear regression, represents vasomotor tone while its slope represents the value of vascular bed resistance. Hence the diameter of the resistance vessel is the relationship between vasomotor tone and vessel diameter.

Since the introduction of TCD, a number of methods have been developed to assess the effective downstream pressure, by extrapolating instantaneous pressure-flow-velocity plots to zero or by calculation of the intercept of diastolic, mean and/or systolic values of pressures and flow-velocity of the middle cerebral artery (Vmca, M1), which is described as ZFP. The effective cerebral perfusion pressure (CPPe) is thus defined by the difference between mean arterial pressure (MAP) and ZFP. Using the CPPe as the driving pressure of the cerebral circulation does not require invasive measurements of intracranial pressure (ICP) and offers advantages in understanding pathophysiology, because changes of the effective downstream pressure irrespective of ICP will also be reflected by this kind of calculation. The inverse of the slope of the arterial blood pressure-Vmca plot, the RAP, has been used as index of CVR. These less invasive methods of assessing cerebral perfusion are well established and have improving accuracy.

In a former investigation, Weyland et al. could support the “alternative model”. Their results confirmed the hypothesis of two Starling resistors in a series connection, one (proximal) at the precapillary level of cerebral resistance vessels (CCPart) and a second (distal) at the level of collapsible cerebral veins (CCPven). Thus, the effective downstream pressure of the cerebral circulation may be determined by either CCP_art, CCP_ven (i.e. ICP), or jugular venous pressure, depending on which one is highest. Thus, the “classical model” must also be considered with limitations.

In patients with arterial hypertension CBF and Vmca will be limited by both:

further increases of ZFP and cerebrovascular resistance (CVR or RAP).

Unfortunately, this has not been tested in greater observational trials.  

Greetings from Rotterdam

Frank 

PS: here some stuff for further reading :

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Burton AC. On the physical equilibrium of small blood vessels. Am J Physiol 1951; 164: 319–329.

Sagawa K, Guyton ACC. Pressure-flow relationships in isolated canine cerebral circulation. Am J Physiol 1961; 200: 711–714.

Permutt S, Riley RL. Hemodynamics of collapsible vessels with tone: The vascular waterfall. J Appl Physiol 1963; 18: 924–932.

Greenfield JC, Tindall GT. Effect of acute increase in intracranial pressure on blood flow in the internal carotid artery of man. J Clin Invest 1965; 44: 1343–1351.

Dewey RC, Pieper HP, Hunt WE. Experimental cerebral hemodynamics. Vasomotor tone, critical closing pressure, and vascular bed resistance. J Neurosurg 1974; 41: 597–606.

Early CB, Dewey RC, Pieper HP, Hunt WE. Dynamic pressure-flow relationships of brain blood flow in the monkey. J Neurosurg 1974; 41: 590–596.

Kontos HA, Wei EP, Raper AJ, Patterson JL. Local mechanism of CO2 action of cat pial arterioles. Stroke 1977; 8: 226–229.

Ehrlich W, Baer RW, Bellamy RF, Randazzo R. Instantaneous femoral artery pressure-flow relations in supine anesthetized dogs and the effect of unilateral elevation of femoral venous pressure. Circ Res 1980; 47: 88–98.

Wei EP, Kontos HA, Patterson JL. Dependence of pial arteriolar response to hypercapnia on vessel size. Am J Physiol 1980; 238: 697–703.

Luce JM, Huseby JS, Kirk W, Butler J. A Starling resistor regulates cerebral venous outflow in dogs. J Appl Physiol 1982; 53: 1496–1503.

Riley RL. A postscript to Circulation of the blood: men and ideas. Circulation 1982; 66: 683–688.

Weyland A, Buhre W, Grund S, Ludwig H, Kazmaier S, Weyland W et al. Cerebrovascular tone rather than intracranial pressure determines the effective downstream pressure of the cerebral circulation in the absence of intracranial hypertension. J Neurosurg Anesthesiol 2000; 12: 210–216.

Magder S. Starling resistor versus compliance. Which explains the zero-flow pressure of a dynamic arterial pressure-flow relation? Circ Res 1990; 67: 209–220.

Carey BJ, Eames PJ, Panerai RB, Potter JF. Carbon dioxide, critical closing pressure and cerebral haemodynamics prior to vasovagal syncope in humans. Clin Sci 2001; 101: 351–358.

Panerai RB. The critical closing pressure of the cerebral circulation. Med Eng Phys 2003; 25: 621–632.

Aaslid R, Lash SR, Bardy GH, Gild WH, Newell DW. Dynamic pressure-flow velocity relationships in the human cerebral circulation. Stroke 2003; 34: 1645–1649.

Czosnyka M, Pickard JD. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg Psychiatr 2004; 75: 813–821.

Kazmaier S, Hanekop GG, Grossmann M, Dörge H, Götze K, Schöndube F et al. Instantaneous diastolic pressure-flow relationship in arterial coronary bypass grafts. Eur J Anaesthesiol 2006; 23: 373–379.