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16 Neurocritical Care Monitoring in ICU: Measurement of the Cerebral…
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TCD and subsequently Mx can assess this rather easily; values of Mx less than or equal to 0 are representative of an intact autoregulatory reserve in which CBFV actively responds to changes in CPP, whereas positive Mx trends state the opposite [23], which provides an example of a patient with disturbed autoregulation, as assessed with Mx.
However, the time-domain calculation of Mx itself does not rely entirely on non­invasive data collection to express autoregulatory reserve; once again, CPP is the difference between ABP and ICP, making Mx somewhat dependent on ICP uctua­tions as a result. Lang etal. [11] attempted to attain Mx with two separate input signals: CPP and ABP, the latter rendering the parameter to be quantiable with non-invasive measures. Although possible to use, Mx determined from ABP is not as sensitive as Mx determined from CPP [19]. Continuing the search for an entirely non-invasive Mx function, Budohoski etal. [12] cited correlations between the sys­tolic (Sx), diastolic (Dx), and mean (Mx) components of the CBFV waveform when using the input signals of either ABP or CPP.Separate analyses yielded the same result: Mx calculated with CPP is the superior predictor of functional patient out­come [1, 12].
16.4 TCD: Benets andLimitations
TCD/TCCS is an important tool to have in neurocritical care units. It is inexpensive, portable, and relatively simple to use once trained in how to do so. TCD examina­tions are as accurate as MRI when assessing vascular pathology [9] and do not require patients to be moved to imaging suites. Additionally, TCD devices can be paired with clinical monitoring software such as ICM+ (Cambridge Enterprise, Ltd.) to return pertinent information about a TBI patient’s state of cerebral auto­regulation that cannot be gleaned from bedside monitors. Without TCD and dedi­cated analytical platforms such as ICM+, mortality and functional outcome could not be determined on the basis of one or two functions (ARI is a more robust predic­tor of mortality than Mx is more sensitive to functional outcome [19, 23, 25]). The benet of both ARI and Mx is that they assign scalar value to cerebral autoregula­tion to the “weighted spatial averages as seen from the aspect of the MCA” [26] when employing the TCD monitoring technique.
Although there is a shortage of “autoregulation markers” [5], the above surro­gates (ARI, Mx) can technically be monitored continuously, as their respective val­ues can be repeatedly calculated over any specied time period during the patient’s neuro-intensive care stay. Therefore, ARI and Mx can be reported in the same fash­ion as ABP and ICP.Despite this important point, TCD and thus its derived param­eters are only intermittently afxed to the patients (<1 hour) due to the relative “clumsiness” and potential disruptiveness of the instrument to routine nursing inter­ventions (i.e., turning the patient, preparing the patient for an X-ray or scan, etc.). TCD is primarily viewed as a research tool and is treated as an accessory to the patient; for example, it is nearly impossible to retain a stable probe position if a
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patient is being re-positioned or examined, as nurses are not obligated to be vigilant over the TCD recording session itself. TCD’s time dependence only permits clini­cians to receive “snapshots” of cerebral hemodynamic activity [1]. Another draw­back of TCD is its reliance on operator validity [10]; even experienced technicians may not agree on the probe placement, depth of the MCA, etc. If the diameter of the MCA were ever to be proven variant, the core of TCD monitoring technology and thus its credibility would be undermined.

16.5 Conclusion

TCD monitoring is entirely non-invasive and allows unique insight into cerebral hemodynamics, particularly through the MCA.The activity within the MCA is cen­tral to the brain’s ability to balance pressure and ow load demands that can be altered by TBI.Although limited by time and technicalities related to its operation, TCD remains a popular tool in neurocritical care centers due to its ability to provide surrogate markers of cerebral autoregulation.

References

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ulation monitoring in acute traumatic brain injury: what’s the evidence? Minerva Anestesiol. 2017;83(8):844–57.
2. Menon DK, Schwab K, Wright DW, Maas AI.Position statement: denition of traumatic brain
injury. Arch Phys Med Rehabil. 2010;91(11):1637–40.
3. Zeiler FA, Donnelly J, Nourallah B, Thelin EP, Calviello L, Smieleweski P, etal. Intra- and
extra-cranial injury burden as drivers of impaired cerebrovascular reactivity in traumatic brain injury. J Neurotrauma. 2018;35(14):1569–77.
4. Budohoski KP, Czosnyka M, Kirkpatrick PJ, Smielewski P, Steiner LA, Pickard JD.Clinical
relevance of cerebral autoregulation following subarachnoid haemorrhage. Nat Rev Neurol. 2013;9(3):152–63.
5. Czosnyka M, Miller C.Monitoring of cerebral autoregulation. Neurocrit Care. 2014;21:95–102.
6. Sorrentino E, Budohoski KP, Kasprowicz M, Smielewski P, Matta B, Pickard JD, etal. Critical
thresholds for transcranial doppler indices of cerebral autoregulation in traumatic brain injury. Neurocrit Care. 2011;14(2):188–93.
7. Cecil S, Chen PM, Callaway SE, Rowland SM, Adler DE, Chen JW.Traumatic brain injury
advanced multimodal neuromonitoring from theory to clinical practice. Crit Care Nurse. 2011;31(2):25–36.
8. Donnelly J, Aries MJ, Czosnyka M.Further understanding of cerebral autoregulation at the
bedside: possible implications for future therapy. Expert Rev Neurother. 2015;15(2):169–85.
9. Panerai RB, Jara JL, Saeed NP, Horseld MA, Robinson T.Dynamic cerebral autoregulation
following acute ischemic stroke: comparison of transcranial Doppler and magnetic resonance imaging techniques. J Cereb Blood Flow Metab. 2015;36:2194–202.
10. Minciotti P, Ceravolo MG, Provinciali L.Inter-examiner variability of transcranial Doppler
procedure and reports: a multicenter survey. Italian Transcranial Doppler Group. Ital J Neurol Sci [Internet]. 1997;18(1):21–30.
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11. Lang EW, Lagopoulos J, Grifth J, Yip K, Mudaliar Y, Mehdorn HM, et al. Noninvasive
cerebrovascular autoregulation assessment in traumatic brain injury: validation and utility. J Neurotrauma. 2003;20(1):69–75.
12. Budohoski KP, Reinhard M, Aries MJH, Czosnyka Z, Smielewski P, Pickard JD, et al.
Monitoring cerebral autoregulation after head injury. Which component of transcranial Doppler ow velocity is optimal? Neurocrit Care. 2012;17(2):211–8.
13. De Riva N, Budohoski KP, Smielewski P, Kasprowicz M, Zweifel C, Steiner LA, et al.
Transcranial doppler pulsatility index: what it is and what it isn’t. Neurocrit Care. 2012;17(1):58–66.
14. Aaslid R, Markwalder T-M, Nornes H.Noninvasive transcranial Doppler ultrasound recording
of ow velocity in basal cerebral arteries. J Neurosurg. 1982;57(6):769–74.
15. Marda M, Prabhakar H.Transcranial Doppler. J Neuroanaesth Crit Care. 2015;2(3):215–20.
16. Aaslid R, Lindegaard KF, Sorteberg W, Nornes H. Cerebral autoregulation dynamics in
humans. Stroke. 1989;20(1):45–52.
17. Tiecks FP, Lam AM, Aaslid R, Newell DW.Comparison of static and dynamic cerebral auto-
regulation measurements. Stroke. 1995;26(6):1014–9.
18. Panerai RB, Haunton VJ, Hanby MF, Salinet ASM, Robinson TG.Statistical criteria for esti-
mation of the cerebral autoregulation index (ARI) at rest. Physiol Meas. 2016;37(5):661–72.
19. Liu X, Czosnyka M, Donnelly J, Budohoski KP, Varsos GV, Nasr N, etal. Comparison of fre-
quency and time domain methods of assessment of cerebral autoregulation in traumatic brain injury. J Cereb Blood Flow Metab. 2015;35(2):248–56.
20. Latka M, Turalska M, Glaubic-Latka M, Kolodziej W, Latka D, West BJ.Phase dynamics in
cerebral autoregulation. Am J Physiol Heart Circ Physiol. 2005;289:2227–9.
21. Diehl RR, Linden D, Lucke D, Berlit P.Phase relationship between cerebral blood ow veloc-
ity and blood pressure: a clinical test of autoregulation. Stroke. 1995;26(10):1801–4.
22. Elting JW, Maurits NM, Aries MJH.Variability of the autoregulation index decreases after
removing the effect of the very low frequency band. Med Eng Phys. 2014;41(1):11–7.
23. Czosnyka M, Smielewski P, Kirkpatrick P, Laing RJ, Menon D, Pickard JD.Continuous assess-
ment of the cerebral vasomotor reactivity in head injury. Neurosurgery. 1997;41(1):11–7.
24. Hlatky R, Furuya Y, Valadka AB, Gonzalez J, Chacko A, Mizutani Y, etal. Dynamic autoregu-
latory response after severe head injury. J Neurosurg. 2002;97(5):1054–61.
25. Schmidt B, Reinhard M, Lezaic V, McLeod DD, Weinhold M, Mattes H, etal. Autoregulation
monitoring and outcome prediction in neurocritical care patients: does one index t all? J Clin Monit Comput. 2016;30(3):367–75.
26. Czosnyka M, Smielewski P, Lavinio A, Pickard JD, Panerai R.An assessment of dynamic
autoregulation from spontaneous uctuations of cerebral blood ow velocity: a comparison of two models, index of autoregulation and mean ow index. Anesth Analg. 2008;106(1):234–9.
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Chapter 17
Neuro-ICU: Cerebral Hemodynamics andTranscranial Doppler (TCD/TCCS) Waveform Interpretation intheMost Common Neurocritical Pathologies
L.LucianoPonceMejia, BahattinB.Ergin, andLucíaRivera Lara
Key Points
1. Adequate brain function requires sufcient, uninterrupted blood ow. Thus, fast-
acting mechanisms are needed to restore blood ow when it drops acutely. Cerebrovascular reactivity is the ability of vascular smooth muscle to change basal tone in response to variations in physiologic parameters, such as arterial blood pressure (ABP), and metabolic factors, such as cerebral carbon dioxide and oxygen levels.
2. The ow velocity decreases as it reaches small vessel branches. Local dimin-
ished vessel diameter (i.e., vasoconstriction) results in a dramatic acceleration in blood ow velocity and a decrease in the pressure. This phenomenon is governed by Bernoulli’s principle, described by Daniel Bernoulli in 1738.
3. Only around 50% of the population has a classic conguration of the circle of
Willis [1]. Stenotic segments are found in more than 25% of people [2]. When the degree of proximal vessel stenosis in the ICA is severe, the blood ow is largely dependent on the collateral vessels. Such collateral circulation tends to be more effective within the circle of Willis because ECA-ICA anastomotic ves­sels are very small and narrow and therefore generate signicant resistance.
L. L. P. Mejia Departments of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
B. B. Ergin Anesthesiology & Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA e-mail: bergin1@jhmi.edu
L. Rivera Lara ( Department of Neurology, Anesthesiology and Critical Care Medicine, The Johns Hopkins School of Medicine, Baltimore, MD, USA e-mail: lriver14@jhmi.edu
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_17
*)
299© Springer Nature Switzerland AG 2022
300
4. The spectral waveform of blood ow velocity can be used to evaluate resistance
to the ow. High-resistance vascular beds are characterized by a waveform with a sharp upstroke accompanied by a relatively abrupt waning in velocity immedi­ately after peak systole with low end-diastolic velocity. Low-resistance wave­forms are characterized by a steadier upstroke, a more gradual decline, and a higher end-diastolic velocity. The cerebral vascular bed is a low-resistance bed. Changes in the resistance, as detected by spectral waveform analysis, can be secondary to local stenosis or to the effects of proximal or distal disease within the insonated vascular bed.
5. The Lindegaard ratio (LR) tends to increase in relation to the degree of vaso-
spasm. Normal reference range is from 1.1 to 2.3 and in the absence of vaso­spasm is <3.
L. L. P. Mejia et al.

17.1 Introduction

Transcranial Doppler (TCD) has gained popularity among physicians because it is a quick, inexpensive, and noninvasive way to evaluate blood ow in the basal cere­bral arteries. The applications of TCD in the neurologically or neurosurgically criti­cally ill patient include vasospasm screening in those with aneurysmal subarachnoid hemorrhage (aSAH) or traumatic brain injury (TBI), detection of embolism after transient ischemic attack or cerebrovascular accident, and evaluation of total cere­bral circulatory arrest in those with brain death. TCD has also been used for estimat­ing cerebral autoregulation and cerebrovascular reactivity and for detecting abnormally high intracranial pressure (ICP).
Interpreting the ndings of TCD requires an understanding of cerebral hemody­namic principles. Cerebral hemodynamics is inuenced by a complicated interac­tion among various factors in critically ill patients, namely, (1) mean arterial blood pressure (MAP), (2) ICP, (3) blood viscosity, (4) degree of proximal vessel stenosis, (5) vessel caliber, (6) degree of collateral circulation, and (7) integrity of cerebral autoregulation. In this chapter, we will review the physiology of cerebral hemody­namics and focus on TCD waveform interpretation.
17.2 Cerebral Blood Flow (CBF) andCerebral Perfusion
Pressure (CPP)
The CPP is equivalent to MAP minus the ICP. The drive to generate blood ow through the cerebral arteries, branches, and capillaries is produced in the left ven­tricle and maintained by the elastic properties of the aorta and extracranial arteries (common carotid artery [CCA] and internal carotid artery [ICA]), resulting in a pulsatile forward pressure. Although the venous blood pressure cannot be
CVRCPP CBF= /
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
discounted, its hemodynamics are far more complex. Often the intracranial venous pressure does not equal the central venous pressure, especially under pathological conditions when an increase in the ICP leads to collapse of the vein wall and a resulting change in ow resistance. Some authors have proposed to use instead of the venous sinus blood pressure (vSBP) because the venous sinuses do not collapse when the ICP rises above that of the vSBP [3]. Nevertheless, the veins that drain into the cerebral sinuses (bridging veins) do collapse when ICP increases, isolating the cerebral venous sinus pressure, an indication that vSBP matches ICP.
301
17.2.1 Cerebrovascular Resistance (CVR)
CVR is maintained mainly by small arteries, resistance vessels, capillaries, and venules. It has been dened as in Eq.17.1. This special pressure–ow relationship is known as Starling resistance, which was rst described in 1912 [4]. The ow in collapsible systems that allows us to dene vSBP as equal to ICP has also been described in detail [57]. Microinvasive methods show a signicant descent in pres­sure from distributing arteries (about 90mmHg) to the arterioles (<30mmHg) [8].
In 1838, using tubes of ne bore in a series of experiments, Jean Leonard Marie Poiseuille (1797–1869) established that ow is inversely proportional to the length of the tube and directly proportional to the pressure gradient and to the fourth power of the tube diameter, the now famed Law of Poiseuille (Eq.17.2):
where ΔP is the pressure difference between the two ends, L is the length of tube (vessel), μ is the dynamic viscosity (hematocrit), Q is the volumetric ow rate (ow velocity), and R is the radius of the vessel. Notably, the radius of the cerebral vessels decreases distally and changes according to physiologic and pathophysiologic states. Consequently, the quantitative use of the Law of Poiseuille is limited. Also, the blood viscosity is non-Newtonian because it is proportional to the velocity of ow. One useful lesson deduced from the Law of Poiseuille is that a modest change in vessel diameter induces a dramatic increase in ow resistance.
DPmLQ pR= 84.../.
(17.1)
(17.2)
17.2.2 Cerebral Autoregulation
Adequate brain function requires sufcient, uninterrupted blood ow. Thus, fast­acting mechanisms are needed to restore blood ow when it drops acutely. Cerebrovascular reactivity is the ability of vascular smooth muscle to change basal
302
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tone in response to variations in physiologic parameters, such as arterial blood pres­sure, and metabolic factors, such as cerebral carbon dioxide and oxygen levels [9]. Cerebral autoregulation is one aspect of cerebrovascular reactivity that involves vas­cular tone changes in response to uctuations in arterial blood pressure [10]. The rst studies of cerebral autoregulation showed that in a normal physiologic state, CBF remains constant when MAP uctuates within 50–150mmHg margin [11]. Modern multimodal monitoring techniques of cerebral autoregulation and cerebro­vascular reactivity have shown that the cerebral autoregulation plateau may be much narrower. In a study of adults with acute subarachnoid hemorrhage, the cerebral autoregulatory plateau was found to be 80–120mmHg [12]. Adjustments of CVR are responsible for maintaining a constant CBF.Thus, CBF is not disturbed by mod­est degrees of stenosis or spasm of proximal vessels. The resistance vessels dilate yielding a lower CVR, which in turn restores CBF [13]. Conversely, a sudden increase in CPP (i.e., MAP) that threatens the integrity of the fragile cerebral capil­laries results in rapid vasoconstriction of the proximal resistance vessels to avoid high transmural pressures. Evidently, more complex and slow metabolic adapta­tions occur in response to abrupt changes in CPP in addition to the fast-myogenic response [1418].
17.2.3 Determination ofCerebrovascular Reactivity Via TCD
In a study of dogs, a 20–25mmHg change in systemic blood pressure produced only a 2.5% change in diameter of the coronary arteries, thanks to their relative stiffness [19]. Cerebral arteries have similar properties. A mean change in blood pressure of 30±16mmHg and a change in end-tidal CO2 (EtCO2) of 14±6mmHg resulted in a mean diameter change in the large cerebral arteries (carotid, middle cerebral artery [MCA], vertebral artery) of less than 4%, but the smaller arteries (anterior cerebral artery, M2 segment of MCA) showed diameter changes as large as 29% to ETCO changes and 21% to blood pressure changes [20, 21]. Hence, as the diameter of the large vessels is relatively stable to changes in blood pressure and CO2, one can assume that the CBF is proportional to the CBF velocity (CBFV). Such changes in CBFV can be measured using TCD technology. Under this premise, CBFV approxi­mates CBF [22]. Cerebrovascular reactivity can be calculated clinically, with the most common methods being (1) dose-controlled CO2 inhalation, (2) acetazolamide injection, and (3) breath-holding index [2325].
17.2.4 Carbon Dioxide Reactivity
Changes in the partial pressure of CO2 (PCO2) cause changes in CVR because CO2 affects the degree of vasodilation of the smaller vessels responsible for regulating CVR.However, the effect of PCO2 on basal cerebral artery diameter is insignicant.
2
()
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
303
By measuring EtCO2 in normal subjects, Markwalder etal. [26] established that ow velocity in the MCA changes 3.4±0.5% per each mmHg change in EtCO2. According to the Poiseuille equation, a change in ow resistance of 3–4% is attained by approximately 1% change in vessel caliber in the resistance vessels. Cerebrovascular reactivity in the neurocritical intensive care unit will be reviewed extensively in a different chapter.
17.3 Physiology ofBlood Vessel Stenosis
The ow velocity decreases as it reaches small vessel branches. Local diminished vessel diameter (i.e., vasoconstriction) results in a dramatic acceleration in blood ow and a decrease in the pressure. This phenomenon is governed by Bernoulli’s principle, described by Daniel Bernoulli in 1738. It states that pressure and velocity in a moving uid have an inverse proportional relationship [27]. Energy is involved in accelerating the uid. Energy is transformed from static energy, namely, pressure, into kinetic energy during acceleration. Such transformation of energy is derived from Bernoulli’s equation (Eq.17.3):
PP rV V
–½=
21 221
DP
2
(17.3)
where ΔP is the pressure difference between the two points with velocities V1 and
V2, respectively, and ρ is the density of blood.
The energy is lost, or rather transformed, in turbulence distal to the stenosis. Note that Bernoulli’s principle takes into consideration the density (viscosity) of the blood. A higher viscosity (hematocrit) results in a higher ΔP. In the brain, there are basically three pathological conditions that can affect blood ow acceleration: (1) large- and mid-size stenosis due to atherosclerotic disease of the extra- and intracra­nial arteries, (2) vasospasm (i.e., subarachnoid hemorrhage), and (3) narrowed con­genital communicating vessels in the circle of Willis (anterior and posterior communicating arteries).
17.3.1 Evaluation ofIntracranial Stenosis by TCD
Using Doppler ultrasound technology to evaluate atherosclerotic disease resulting in stenosis of the CCA bifurcation predates TCD [28]. The development of TCD technology with a transorbital approach of the carotid siphon made possible the evaluation of intracranial stenotic disease with an overall accuracy of 88%, a 95% specicity, and a 73% sensitivity when compared to angiography [29]. The trans­temporal and suboccipital approaches were later described with a correlation coef­cient of 0.89 (p=0.0001) [30, 31]. A proposed model of unilateral carotid artery
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stenosis suggests that for a severe unilateral stenosis of the right carotid artery, the partial pressure of oxygen in the brain area at risk can be restored only if the corre­sponding cerebral resistance is signicantly decreased and if the circle of Willis is complete [32]. Another report showed no preoperative difference in number of intracerebral arteries with reverse ow between symptomatic and asymptomatic patients with severe unilateral carotid stenosis. In contrast, pulsatility index, cere­brovascular reactivity, and ow acceleration on the side of stenosis were signi­cantly lower in symptomatic patients. After surgery, all TCD parameters improved signicantly in both symptomatic and asymptomatic patients [33]. The Doppler ndings showed increased ow velocity at the site of stenosis, a decrease in velocity with a dampened waveform distally, and at least a 20–30mmHg pressure loss. This phenomenon has a parabolic relationship. Stenotic atherosclerotic lesions have obvious hemodynamic effects. The inverse correlation of low velocity obtained by TCD as a function of lumen dimension has been reported in patients with intracra­nial artery disease when the measurements of diameter were corrected by angiogra­phy [34]. Such inverse correlation ndings appear to deviate less in atherosclerotic disease than in vasospasm.
17.3.2 Collateral Flow
Only around 50% of the population has a classic conguration of the circle of Willis [1]. Stenotic segments are found in more than 25% of people [2]. When the degree of proximal vessel stenosis in the ICA is severe, the blood ow is largely dependent on the collateral vessels. Such collateral circulation tends to be more effective within the circle of Willis, because ECA-ICA anastomotic vessels are very small and narrow and therefore generate signicant resistance. Variability in the pressure of the various collateral connecting vessels (stumps) in the circle of Willis has been reported to be high, ranging from as low as 10mmHg to almost equating the systemic blood pressure [35]. The resistance to ow in a given collat­eral connection is determined by vessel diameter, length, and viscosity. The effect of the circle of Willis conguration on cerebrovascular hemodynamics and the dis­tribution of ow appears to be highly variable from individual to individual [36,
37]. Consequently, studying its inuence is very difcult [3840]. One of the most
common noninvasive TCD techniques used to assess collateral ow within circle segments uses carotid compression [41]. Because blood volume is directly propor­tional to ow velocity, common carotid compression measures its effect on blood ow velocity in the ipsilateral posterior cerebral artery and contralateral anterior cerebral artery. Thus, this test shows that the communicating arteries are open and to what degree. The presence of chronic atherosclerotic lesion and its effect on ow velocity in the circle of Willis has also been studied. Researchers have shown increased, reversed, and crossover ow in the different compensating vessels ipsi­lateral and contralateral to the atherosclerotic lesion, sometimes greater than 1.5
CVP=∆ /
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
305
times the velocity in the ipsilateral MCA when the extracranial ICA occlusion reached about 90% [30, 34].
17.3.3 Elastic Reservoir (“Windkessel Effect”)
It is important to remember that the properties described so far (resistance, turbu­lence, etc.) and their effects on ow apply only to a model with a static pressure– ow relationship. However, the pulsatile nature of the pressure in extra- and intracranial vessels results in a dynamic pressure–ow relationship because these vessels are elastic. The most important dynamic relationship is known as the “Windkessel” effect. The Windkessel model described by Otto Frank [42, 43] denes the hemodynamics of the arterial system in terms of resistance and compli­ance. It describes the aortic pressure decline during diastole but not entirely so dur­ing systole. Impedance was proposed as a third component of the Windkessel model. The heart ejects blood intermittently; however, the ow is more continuous as the blood pressure pulsates because the elasticity of the arterial system acts as a reser­voir of the energy supplied during systole, thus making the system more efcient. This model can then predict the classic shape of the ow waveform seen in a pulsa­tile system [42, 43]. Windkessel is roughly translated from German to English as “air chamber,” drawing the analogy with the air chamber used in re engines in the eighteenth century [44]. CBF waveforms obtained by TCD are consistent with low­resistance ow, which changes in pathological states. The Windkessel model is a lumped model and therefore not appropriate for the evaluation of wave travel, but it is a fair approximation of ventricular afterload.
Compliance (C) is the ability of a vessel to distend and increase volume with increasing transmural pressure or the tendency to resist recoil toward its original dimensions on application of a distending or compressing force. It is dened as (Eq.17.4)
(17.4)
The following are scenarios in which the effect of compliance markedly affects the ow velocity waveform. (1) Proximal stenosis resulting in a dampened velocity waveform [34, 45]. The Windkessel effect produces a more smoothed waveform because of the increased inow resistance. (2) Size and amount of arteriovenous malformation feeders. Because arteriovenous malformations have high volume stiffness and very low ow resistance, they result in a dampened waveform. (3) Hypocapnia results in increased ow velocity pulsatility [26]. Low PCO2 leads to vasoconstriction that increases resistance, revealing the Windkessel effect. (4) Pathological ICP elevation also results in a very pulsatile waveform [46]. Two fac- tors have been proposed to explain this phenomenon. First, the pulsatility of the CPP increases with increasing ICP, and second, the total volume compliance increases so that more blood is required in systole to ll the “Windkessel.”