Hemodynamics and Functional Tests

3


Intracranial Hemodynamics and Functional Tests


Analysis of Cerebral Blood Flow


Autoregulation


Testing of Autoregulation


Neurovascular Coupling


Testing of Neurovascular Coupling


Metabolic Coupling


Testing of Metabolic Coupling


Other Tests to Assess Differences Between the Right and Left Sides as Markers of Impaired Collateral Function


Parameters of Cerebral Hemodynamics


Cerebral Blood Flow Velocity


Resistance Indices


Cerebral Blood Flow Volume


Cerebral Circulation Time


Cerebral Blood Volume


Analysis of Cerebral Blood Flow


In contrast to many other organ systems, the human brain has several characteristics that are important in analyzing and interpreting cerebral perfusion. At rest, the brain receives a high proportion of the total cardiac output—in the order of 15–20%. The global cerebral blood flow (CBF) in an adult amounts to 700–800 mL/min, i.e., 13 mL/s or 55 mL/100 mg per minute assuming a brain weight of 1,400 g. About of 75% of the global CBF derives from the internal carotid arteries (ICAs) and the remaining 25% from both vertebral arteries (VAs) (Schöning et al 1994).


The ideal way to assess brain perfusion would be to analyze CBF directly. However, conventional Doppler flow velocity examination only generally permits flow velocity analysis of proximal arterial or venous vessel segments. CBF and flow velocity are not equal but correlate strongly with one other. A rising CBF causes rising blood flow velocities, and a low CBF correlates with low blood flow velocities. However, there are other important factors that have to be considered: Flow velocity correlates with the size of a vessel’s vascular territory despite the fact that the vessel’s diameter is adapted to it. For example, flow velocities in the middle cerebral artery (MCA), which supplies the largest cerebral territory, are higher than in the anterior cerebral artery (ACA) and posterior cerebral artery (PCA). In the anatomic variation with one A1-ACA segment providing blood supply to both ACA territories, its flow velocity is similar to or even higher than that of the ipsilateral M1-MCA.


Flow velocity also depends on vessel size. Local vessel narrowing will lead to increased velocities. Vessel dilatation, for example in hypertensive dilative vasculopathy or aneurysm formation, results in decreased flow velocities.


Other factors have more general effects. Anemia leads to a generalized increase of flow velocities. Flow velocities tend to decrease with increasing age, which is mainly attributed to brain parenchymal loss and subsequent reduction of CBF but also to vessel dilation. Under pathologic conditions chronological aspects have to be considered. For example, acute-phase flow assessment in ischemic stroke with intracranial large-vessel occlusion often shows reduced flow velocities in the preocclusive vessel segments. In the subsequent hyperemic phase after recanalization, increased velocities can be seen. However, the final or chronic state might show a reduction of flow velocity and an increase of pulsatility, depending on the extent of the remaining parenchymal defect (“no brain, no flow”).


As brain tissue has virtually no energy reserves, changes in perfusion lead to an immediate alteration in brain function. Therefore, many regulatory processes (these are listed and discussed below) exist to ensure a continuous and constant blood supply. Probably more than any other organ system, the brain needs to be constantly perfused for optimal function. However, the heart, which is responsible for blood supply and blood drainage, is a pulsatile pump. The arteries are the solution to this problem: with their elastic vessel walls they are capable of storing a considerable amount of blood during the systolic phase that is then released into the circulation during diastole (Windkessel function). This leads to an almost continuous blood flow in the periphery.


For easier understanding of the flow pattern seen during insonation of proximal arteries, we now introduce a simple model (Fig. A3.1). A filled rain barrel discharges water through a rigid pipe. To imitate the pulsatile action of the heart, a tap placed at the beginning of the pipe is repeatedly opened and closed. Flow analysis, in analogy to ultrasound analysis of proximal arterial blood vessels, is performed in the central segment of this pipe. The measured flow is pulsatile, with a high flow velocity when the tap is open (systole) and no flow when the tap is closed (diastole). If an elastic hose is used instead of a rigid pipe the flow profile will look different, i.e., more like the arterial blood flow profile in nonparenchymal organs (Fig. A3.2). When the tap is closed the elastic hose allows a continuous flow comparable with the arterial Windkessel function. If a second peripheral tap is added to the system, a microcirculation (as found in parenchymal organs such as the brain and kidneys) can be introduced into the model (Fig. A3.3): A reduction of outflow (microcirculation tap almost closed) will lead to reduced systolic flow velocities but distinctly lowered diastolic flow velocities and subsequently higher pulsatility. Opening of the microcirculation tap will lead to a reduction in peripheral resistance, resulting in slightly higher systolic flow velocities and distinctly higher diastolic velocities, i.e., reduced pulsatility.




In addition to the mechanisms explained above, the Doppler waveform and pulsatility are also modulated by the quality of cardiac function, which can be altered by conditions like atrial fibrillation, congestive heart failure, aortic valve stenosis, insufficiency, or cardiomyopathy (Fig. A3.4 and Fig. A3.5).


Autoregulation


In contrast to other organ systems, but analogous to the kidney, the brain has an autoregulatory system that ensures constant tissue perfusion. Factors that influence cerebral perfusion are the cerebral perfusion pressure (CPP = mean arterial blood pressure [ABP] − intracranial pressure [ICP]) and the cerebrovascular resistance (CVR), determined by the functional status of the arteriolar vessels of the cerebral microcirculation. Under normal physiologic circumstances the ICP at rest is ~10–15 mm Hg and the resulting CPP is therefore only slightly lower than the ABP.


CBF = ABP/CVR (Ohm’s law of hemodynamics).



The above formula shows that CBF can be kept almost stable during changes in ABP if compensatory alterations are made in the cerebrovascular resistance, i.e., the microcirculation. Low blood pressure requires a reduction of resistance, i.e., a dilation of the peripheral arterial vessels. High blood pressure requires peripheral vasoconstriction. As CBF is closely related to the blood flow velocities in the main arteries supplying the brain, the above mechanism will result in stable flow velocities during changes in blood pressure (Diehl 2002). However, this mechanism only works under physiologic conditions within a certain range of blood pressure (autoregulatory plateau), as changes in the diameter of the peripheral arterial vessels only occur over a certain range. Above and below this range the mechanism fails and blood pressure and CBF are directly coupled (Fig. A3.6). If regional autoregulation is abolished or impaired, for example in ischemic stroke, this also implies direct coupling of cerebral perfusion and blood pressure. Therefore, a reduction in blood pressure in impaired autoregulation will lead to a reduction of brain perfusion, which should be avoided. Conversely, in acute stroke normal or slightly raised blood pressure is desired. For further reading see also Chapter 5, “Collateral Pathways.”



Testing of Autoregulation


For cerebral functional and regulatory testing, the transcranial Doppler (TCD) method is preferred; ultrasound probe holding systems are commercially available which permit continuous monitoring over time without the risk of change in probe position. In contrast with current duplex ultrasound systems, TCD permits simultaneous measurement in more than one blood vessel, i.e., bilateral monitoring is possible (Fig. A3.7).


Several methods of autoregulatory testing by means of blood pressure alteration have been proposed. Aaslid and coworkers (1989) published a thigh-cuffmethod in which sudden blood pressure drops can be induced. Two thigh cuffs are inflated above systolic blood pressure values for more than 2 minutes, causing temporary leg ischemia. A sudden cuff release results in leg hyperemia and an ~20% systemic blood pressure drop lasting 10 seconds. In normal autoregulation, this maneuver leads to an initial reduction of blood flow velocity within the MCA. Compensatory autoregulatory flow increase starts after 1 second and flow velocities reach normal values after 5 seconds. Other published methods are the performance of a standardized Valsalva maneuver and the analysis of spontaneous blood pressure oscillations. The former test comprises expiration into a tube containing a closed pressure valve over 15 seconds, resulting in a transient blood pressure reduction as well as a less pronounced temporary reduction of blood flow velocity within the MCA, caused by the autoregulatory response (Tiecks et al 1996). The latter method analyzes spontaneous blood pressure oscillations (M-waves) or oscillations induced by slow breathing. High frequencies of more than 0.2 Hz were found to result in virtually direct changes of MCA flow velocity. Blood pressure oscillations at lower frequencies led to phase-shifted MCA velocity changes of up to 70°, i.e., an autoregulatory response was observed (Diehl 2002, Diehl et al 1995).






All three reported methods have been shown to detect impaired autoregulation in patients with, for example, a high-grade ICA stenosis. So far, these methods are mostly used in specialized centers either because additional continuous blood pressure monitoring is required (thigh-cuffand Valsalva method) or because commercial evaluation software is not available (spontaneous oscillation method).


Neurovascular Coupling


Coupling of activity and blood flow is a ubiquitous mechanism of all organ systems. In neurovascular coupling of the brain, a raised metabolic demand, due to activation of particular brain regions, for example, leads to an increase of blood flow and a proportional rise of blood flow velocity. A typical example of this mechanism is the use of a visual stimulus paradigm under continuous insonation of the PCA (Fig. A3.8). While the detailed translational mechanisms from activated brain cells to increased flow are still being extensively studied, the effector mechanism is a dilatation of the peripheral arteries (resistance vessels), i.e., the microcirculation, which leads to a flow increase (as explained in Fig. A3.3).


Testing of Neurovascular Coupling


A simple and easily applicable method is the visual stimulation test (visual evoked Doppler [VED]), in which repetitive visual stimuli are used and the flow velocity in the PCA is analyzed. As a stimulus, a flashing light or any other standardized visual stimulus that can be applied by means of a computer screen can be used. To improve signal-to-noise ratio, repetitive averaging, comparable to the electric visual evoked potential, is used (Sturzenegger et al 1996). As the PCA mainly supplies the visual cortex, only a few repetitive stimuli (we recommend 20–40 stimuli) are necessary to achieve evaluable curves (Fig. A3.9). For evaluation, the baseline velocity is adjusted to 100% and the flow increase assessed in percent over baseline levels. From these curves, peak increase and time to peak can be derived and used for evaluation. Diehl and Berlit reported a mean increase of 40 ± 8% in the Doppler sonographic P2-PCA segment in a group of 30 healthy volunteers (Diehl and Berlit 1996). Apart from studying the physiology of neurovascular coupling (Rosengarten et al 2006) this method has also been used to study anterior and posterior circulation cerebral ischemia (Lin et al 2011), in different states of brain dysfunction including suspected vegetative states (Becker et al1996), migraineurs (Thie et al 1990, Peca et al 2013), amyloid angiopathy (Smith et al 2008), and more recently, pre-eclampsia (Janzarik et al 2014).


Jun 20, 2018 | Posted by in NEUROSURGERY | Comments Off on Hemodynamics and Functional Tests

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