scholarly journals Variability and Fractal Analysis of Middle Cerebral Artery Blood Flow Velocity and Arterial Blood Pressure in Subarachnoid Hemorrhage

2007 ◽  
Vol 28 (1) ◽  
pp. 64-73 ◽  
Author(s):  
Martin Soehle ◽  
Marek Czosnyka ◽  
Doris A Chatfield ◽  
Andreas Hoeft ◽  
Alonso Peña
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Fractal Analysis ◽  
Blood Flow Velocity ◽  
Artery Blood Flow ◽  
Arterial Blood ◽  
Hurst Coefficient

Higher biologic systems operate far from equilibrium resulting in order, complexity, fluctuation of inherent parameters, and dissipation of energy. According to the decomplexification theory, disease is characterized by a loss of system complexity. We analyzed such complexity in patients after subarachnoid hemorrhage (SAH), by applying the standard technique of variability analysis and the novel method of fractal analysis to middle cerebral artery blood flow velocity (FV) and arterial blood pressure (ABP). In 31 SAH –patients, FV (using transcranial Doppler sonography) and direct ABP were measured. The standard deviations (s.d.) and coefficients of variation (CV = relative s.d.) for FV and ABP time series of length 210 secs were calculated as measures of variability. The spectral index βlow and the Hurst coefficient HbdSWV were analyzed as fractal measures. Outcome was assessed 1 year after SAH according to the Glasgow Outcome Scale (GOS). Both FV (βlow = 2.2±0.4, mean±s.d.) and ABP (βlow = 2.3±0.4) were classified as nonstationary (fractal Brownian motion) signals. FV showed significantly ( P <0.05) higher variability (CV = 7.2±2.5%) and Hurst coefficient ( HbdSWV = 0.26±0.13) as compared with ABP (CV = 5.5±2.7%, HbdSWV = 0.19±0.11). Better outcome (GOS) correlated significantly ( P <0.05) with higher s.d. of FV (Spearman's rs = 0.51, rs2 = 0.26) and ABP ( rs = 0.57, rs2 = 0.32), as well as with a higher Hurst coefficient of ABP ( rs = 0.46, rs2 = 0.21). Cerebral vasospasm reduced CV of FV, but left HbdSWV unchanged. FV and ABP fluctuated markedly despite homeostatic control. A reduced variability of FV and ABP might indicate a loss of complexity and was associated with a less favorable outcome. Therefore, the decomplexification theory of illness may apply to SAH.

Effects of Sufentanil on Cerebral Hemodynamics and Intracranial Pressure in Patients with Brain Injury

1995 ◽  
Vol 83 (4) ◽  
pp. 721-726. ◽  
Author(s):  
Christian Werner ◽  
Eberhard Kochs ◽  
Hanswerner Bause ◽  
William E. Hoffman ◽  
Jochen Schulte am Esch
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Artery Blood Flow ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Group 2 ◽  
Group 1

Background The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale &lt; 6). Methods Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. Results Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP &gt; 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. Conclusions The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.

Disassociation of static and dynamic cerebral autoregulatory performance in healthy volunteers after lipopolysaccharide infusion and in patients with sepsis

2012 ◽  
Vol 303 (11) ◽  
pp. R1127-R1135 ◽  
Author(s):  
Ronan M. G. Berg ◽  
Ronni R. Plovsing ◽  
Andreas Ronit ◽  
Damian M. Bailey ◽  
Niels-Henrik Holstein-Rathlou ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Healthy Volunteers ◽  
Flow Velocity ◽  
Phase Difference ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Artery Blood Flow

Sepsis is frequently complicated by brain dysfunction, which may be associated with disturbances in cerebral autoregulation, rendering the brain susceptible to hypoperfusion and hyperperfusion. The purpose of the present study was to assess static and dynamic cerebral autoregulation 1) in a human experimental model of the systemic inflammatory response during early sepsis and 2) in patients with advanced sepsis. Cerebral autoregulation was tested using transcranial Doppler ultrasound in healthy volunteers ( n = 9) before and after LPS infusion and in patients with sepsis ( n = 16). Static autoregulation was tested by norepinephrine infusion and dynamic autoregulation by transfer function analysis (TFA) of spontaneous oscillations between mean arterial blood pressure and middle cerebral artery blood flow velocity in the low frequency range (0.07–0.20 Hz). Static autoregulatory performance after LPS infusion and in patients with sepsis was similar to values in healthy volunteers at baseline. In contrast, TFA showed decreased gain and an increased phase difference between blood pressure and middle cerebral artery blood flow velocity after LPS (both P < 0.01 vs. baseline); patients exhibited similar gain but lower phase difference values ( P < 0.01 vs. baseline and LPS), indicating a slower dynamic autoregulatory response. Our findings imply that static and dynamic cerebral autoregulatory performance may disassociate in sepsis; thus static autoregulation was maintained both after LPS and in patients with sepsis, whereas dynamic autoregulation was enhanced after LPS and impaired with a prolonged response time in patients. Hence, acute surges in blood pressure may adversely affect cerebral perfusion in patients with sepsis.

Complexity of middle cerebral artery blood flow velocity: effects of tilt and autonomic failure

1997 ◽  
Vol 273 (5) ◽  
pp. H2209-H2216 ◽  
Author(s):  
A. P. Blaber ◽  
R. L. Bondar ◽  
F. Stein ◽  
P. T. Dunphy ◽  
P. Moradshahi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Autonomic Failure ◽  
Systemic Blood Pressure ◽  
Arterial Blood ◽  
Different Response

We examined spectral fractal characteristics of middle cerebral artery (MCA) mean blood flow velocity (MFV) and mean arterial blood pressure adjusted to the level of the brain (MAPbrain) during graded tilt (5 min supine, −10°, 10°, 30°, 60°, −10°, supine) in eight autonomic failure patients and age- and sex-matched controls. From supine to 60°, patients had a larger drop in MAPbrain (62 ± 4.7 vs. 23 ± 4.5 mmHg, P < 0.001; means ± SE) and MFV (16.4 ± 3.8 vs. 7.0 ± 2.5 cm/s, P < 0.001) than in controls. From supine to 60°, there was a trend toward a decrease in the slope of the fractal component (β) of MFV (MFV-β) in both the patients and the controls, but only the patients had a significant decrease in MFV-β (supine: patient = 2.21 ± 0.18, control = 1.99 ± 0.60; 60°: patient = 1.46 ± 0.24, control = 1.62 ± 0.19). The β value of MAPbrain(MAPbrain-β; 2.19 ± 0.05) was not significantly different between patients and controls and did not change with tilt. High and low degrees of regulatory complexity are indicated by values of β close to 1.0 and 2.0, respectively. The increase in fractal complexity of cerebral MFV in the patients with tilt suggests an increase in the degree of autoregulation in the patients. This may be related to the drop in MAPbrain. The different response of MFV-β compared with that of MAPbrain-β also indicates that MFV-β is related to the regulation of cerebral vascular resistance and not systemic blood pressure.

Decrease of blood flow velocity in the middle cerebral artery after stellate ganglion block following aneurysmal subarachnoid hemorrhage: a potential vasospasm treatment?

2020 ◽  
Vol 133 (3) ◽  
pp. 773-779
Author(s):  
Christopher Wendel ◽  
Ricardo Scheibe ◽  
Sören Wagner ◽  
Wiebke Tangemann ◽  
Hans Henkes ◽  
...  
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Neurological Deficit ◽  
Blood Flow Velocity ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Stellate Ganglion ◽  
Stellate Ganglion Block ◽  
Ganglion Block

OBJECTIVECerebral vasospasm (CV) is a delayed, sustained contraction of the cerebral arteries that tends to occur 3–14 days after aneurysmal subarachnoid hemorrhage (aSAH) from a ruptured aneurysm. Vasospasm potentially leads to delayed cerebral ischemia, and despite medical treatment, 1 of 3 patients suffer a persistent neurological deficit. Bedside transcranial Doppler (TCD) ultrasonography is used to indirectly detect CV through recognition of an increase in cerebral blood flow velocity (CBFV). The present study aimed to use TCD ultrasonography to monitor how CBFV changes on both the ipsi- and contralateral sides of the brain in the first 24 hours after patients have received a stellate ganglion block (SGB) to treat CV that persists despite maximum standard therapy.METHODSThe data were culled from records of patients treated between 2013 and 2017. Patients were included if an SGB was administered following aSAH, whose CBFV was ≥ 120 cm/sec and who had either a focal neurological deficit or reduced consciousness despite having received medical treatment and blood pressure management. The SGB was performed on the side where the highest CBFV had been recorded with 8–10 ml ropivacaine 0.2%. The patient’s CBFV was reassessed after 2 and 24 hours.RESULTSThirty-seven patients (male/female ratio 18:19), age 17–70 years (mean age 49.9 ± 11.1), who harbored 13 clipped and 22 coiled aneurysms (1 patient received both a coil and a clip, and 3 patients had 3 untreated aneurysms) had at least one SGB. Patients received up to 4 SGBs, and thus the study comprised a total of 76 SGBs.After the first SGB, CBFV decreased in 80.5% of patients after 2 hours, from a mean of 160.3 ± 28.2 cm/sec to 127.5 ± 34.3 cm/sec (p < 0.001), and it further decreased in 63.4% after 24 hours to 137.2 ± 38.2 cm/sec (p = 0.007). A similar significant effect was found for the subsequent SGB. Adding clonidine showed no significant effect on either the onset or the duration of the SGB. Contralateral middle cerebral artery (MCA) blood flow was not reduced by the SGB.CONCLUSIONSTo the authors’ knowledge, this is the largest study on the effects of administering an SGB to aSAH patients after aneurysm rupture. The data showed a significant reduction in ipsilateral CBFV (MCA 20.5%) after SGB, lasting in about two-thirds of cases for over 24 hours with no major complications resulting from the SGB.

Diurnal variation in time to presyncope and associated circulatory changes during a controlled orthostatic challenge

2010 ◽  
Vol 299 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
N. C. S. Lewis ◽  
G. Atkinson ◽  
S. J. E. Lucas ◽  
E. J. M. Grant ◽  
H. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diurnal Variation ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Orthostatic Challenge ◽  
Arterial Blood ◽  
Neurally Mediated Syncope

Epidemiological data indicate that the risk of neurally mediated syncope is substantially higher in the morning. Syncope is precipitated by cerebral hypoperfusion, yet no chronobiological experiment has been undertaken to examine whether the major circulatory factors, which influence perfusion, show diurnal variation during a controlled orthostatic challenge. Therefore, we examined the diurnal variation in orthostatic tolerance and circulatory function measured at baseline and at presyncope. In a repeated-measures experiment, conducted at 0600 and 1600, 17 normotensive volunteers, aged 26 ± 4 yr (mean ± SD), rested supine at baseline and then underwent a 60° head-up tilt with 5-min incremental stages of lower body negative pressure until standardized symptoms of presyncope were apparent. Pretest hydration status was similar at both times of day. Continuous beat-to-beat measurements of cerebral blood flow velocity, blood pressure, heart rate, stroke volume, cardiac output, and end-tidal Pco2 were obtained. At baseline, mean cerebral blood flow velocity was 9 ± 2 cm/s (15%) lower in the morning than the afternoon ( P < 0.0001). The mean time to presyncope was shorter in the morning than in the afternoon (27.2 ± 10.5 min vs. 33.1 ± 7.9 min; 95% CI: 0.4 to 11.4 min, P = 0.01). All measurements made at presyncope did not show diurnal variation ( P > 0.05), but the changes over time (from baseline to presyncope time) in arterial blood pressure, estimated peripheral vascular resistance, and α-index baroreflex sensitivity were greater during the morning tests ( P < 0.05). These data indicate that tolerance to an incremental orthostatic challenge is markedly reduced in the morning due to diurnal variations in the time-based decline in blood pressure and the initial cerebral blood flow velocity “reserve” rather than the circulatory status at eventual presyncope. Such information may be used to help identify individuals who are particularly prone to orthostatic intolerance in the morning.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

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