Mean Cerebral Blood Flow Velocity Research Articles

Cerebral Blood Flow Velocity Changes After Bovine Natural Surfactant Instillation

To determine the effects of bovine natural surfactant (beractant) instillation on cerebral hemodynamics in preterm infants with respiratory distress syndrome (RDS). Preterm infants who required surfactant for RDS were enrolled. Cerebral blood flow velocity (CBFV) waveforms from the pericallosal artery were analyzed by pulsed Doppler ultrasonography with the anterior fontanel serving as an acoustic window. CBFV was measured before and at 5, 10, 20, and 30 minutes after the first dose of a bolus instillation of surfactant in four aliquots. Simultaneously with CBFV measurements, mean blood pressure (MBP), heart rate, and ventilator settings were recorded. pH, PACO2, and PAO2 before and at 30 minutes after surfactant administration were also determined. The 30 enrolled preterm infants had a mean birth weight of 973 gm (513 to 1996 gm) and a mean gestational age of 27 weeks (23 to 33 weeks). Mean postnatal age at surfactant administration was 4.7 +/- 2.7 hours. There were no significant changes in pH and PACO2 before and at 30 minutes after surfactant (before surfactant: mean pH of 7.29 +/- 0.07 and mean PACO2 of 44.4 +/- 7.1 torr; after surfactant: mean pH of 7.31 +/- 0.07 and mean PACO2 of 42.7 +/- 8.3 torr). PAO2 increased significantly from a pre-surfactant mean of 83 torr to 130 torr at 30 minutes after surfactant (p < 0.05), with no significant changes in mean airway pressure. There were no significant changes in MBP, heart rate, mean CBFV, peak systolic flow velocity, and diastolic flow velocity before and after surfactant instillation regardless of gestational age. Individual changes in mean CBFV were related to MBP changes (p < 0.001, linear mixed models with random effects). In low birth weight infants with RDS, bovine surfactant instillation is not associated with a significant alteration in cerebral hemodynamics. However, the direct relationship between CBFV and MBP is consistent with the reported pressure-passive cerebral circulation in sick preterm infants.

Spontaneous fluctuations in cerebral blood flow: insights from extended-duration recordings in humans.

To determine the dependence of cerebral blood flow (CBF) on arterial pressure over prolonged time periods, we measured beat-to-beat changes in mean CBF velocity in the middle cerebral artery (transcranial Doppler) and mean arterial pressure (Finapres) continuously for 2 h in six healthy subjects (5 men and 1 woman, 18-40 yr old) during supine rest. Fluctuations in velocity and pressure were quantified by the range [(peak - trough)/mean] and coefficients of variation (SD/mean) in the time domain and by spectral analysis in the frequency domain. Mean velocity and pressure over the 2-h recordings were 60 +/- 7 cm/s and 83 +/- 8 mmHg, associated with ranges of 77 +/- 8 and 89 +/- 10% and coefficients of variation of 9.3 +/- 2.2 and 7.9 +/- 2.3%, respectively. Spectral power of the velocity and pressure was predominantly distributed in the frequency range of 0.00014-0.1 Hz and increased inversely with frequency, indicating characteristics of an inverse power law (1/f(alpha)). However, linear regression on a log-log scale revealed that the slope of spectral power of pressure and velocity was steeper in the high-frequency (0.02-0.5 Hz) than in the low-frequency range (0.002-0.02 Hz), suggesting different regulatory mechanisms in these two frequency ranges. Furthermore, the spectral slope of pressure was significantly steeper than that of velocity in the low-frequency range, consistent with the low transfer function gain and low coherence estimated at these frequencies. We conclude that 1) long-term fluctuations in CBF velocity are prominent and similar to those observed in arterial pressure, 2) spectral power of CBF velocity reveals characteristics of 1/f(alpha), and 3) cerebral attenuation of oscillations in CBF velocity in response to changes in pressure may be more effective at low than that at high frequencies, emphasizing the frequency dependence of cerebral autoregulation.

Cerebral vascular effects of aortovenous cannulations for pediatric cardiopulmonary bypass

Background. The effects of aortovenous cannulations for pediatric cardiopulmonary bypass on cerebral blood flow velocity (CBFV) and electroencephalography (EEG) were evaluated.Methods. CBFV and EEG were continuously recorded before (baseline), during, and after cannulations until initiation of cooling (mean ± 95% confidence interval). Vasopressors and/or volume replacement were administered if mean arterial pressure (MAP) decreased below 35 mm Hg. Cannulation-related EEG slowing was used as a criterion for electrocortical alteration.Results. We studied 124 children (3 days to 17 years of age). Aortic and venous cannulations decreased mean CBFV by 10 ± 3% and 13 ± 4%, respectively, from baseline (p < 0.001). MAP diminished (p < 0.01) by 8 ± 3% and 12 ± 4%, respectively, from precannulation values (53 ± 2 mm Hg). Right atrial cannulation, which was often chosen because the patient was hemodynamically unstable, was more frequently associated with pharmacologic intervention when compared with superior vena cava (SVC) cannulation (p < 0.01). Transient EEG alterations (n = 20) were associated with persistently low MAP (< 30 mm Hg), low CBFV (< 69%), and aortic (n = 4) or SVC (n = 7) cannula malposition. Infants with right atrial cannulation and intervention had more frequent EEG alterations (p = 0.04). Patients requiring intervention were younger (p < 0.01) and had longer hospital stay (p < 0.01) than those without intervention.Conclusions. Cerebral effects of cannulations are greater in young infants. This was found to be associated with low MAP during heart manipulation or consequence of cannula malpositions.

Recent Developments in the Management of Neonatal Hyperbilirubinemia

After completing this article, readers should be able to: 1. Describe the morbidity associated with exchange transfusion used to treat neonatal hyperbilirubinemia. 2. Explain how phototherapy affects bilirubin. 3. Describe potential toxicities of phototherapy. 4. Explain the role of carboxyhemoglobin in hemolysis. 5. Delineate the guidelines for administering intravenous immunoglobulin to healthy ABO-incompatible Coombs-positive neonates. 6. Describe the action of protoporphyrins on bilirubin. Recent clinical trends toward early discharge coupled with a new, more relaxed, “kinder, gentler approach” to the treatment of newborn hyperbilirubinemia have thrust concerns about bilirubin-related toxicity once again to the forefront of neonatologists’ consciousness. In recent years we even have witnessed a resurgence of kernicterus, which had been rendered almost nonexistent in the 1970s and 1980s. Although exchange transfusion is the oldest and most effective method of treating hyperbilirubinemia, mortality associated with this therapy has been reported to be between 0.3% and 1.2% in healthy infants and as high as 10% to 25% in sicker preterm infants. Furthermore, potential morbidity related to exchange transfusion remains significant and includes anemia, apnea, bradycardia, hypothermia, sepsis, necrotizing enterocolitis, thromboembolic phenomena, graft versus host disease, transient metabolic abnormalities, and thrombocytopenia. Accordingly, it behooves us to re-evaluate other therapeutic modalities for hyperbilirubinemia that may be equally efficacious but less invasive. Ever since the 1950s, when Sister Ward of Rochford General Hospital in Essex noted that a jaundiced baby’s skin had “faded” in natural sunlight, physicians have been searching for artificial light sources that might be used safely to treat neonatal hyperbilirubinemia. Phototherapy, which has become the standard of care, has had such a dramatic impact that a recent editorial raised the concern that exchange transfusions are becoming extinct and lamented the fact that future generations of house officers may not receive adequate training in this procedure. Under the effects of phototherapy light with maximal irradiance in the …

Persistence of cerebral hemodynamic changes in patients with eclampsia: A report of three cases

Objective: This study was undertaken to compare the persistence of changes in estimated cerebral perfusion pressure and the resistance area product, an index of cerebrovascular resistance, in women with preeclampsia and women with eclampsia. Study Design: The maternal middle cerebral artery was evaluated by transcranial Doppler ultrasonography in 6 patients with severe preeclampsia and 3 women with eclampsia, and cerebral blood flow velocities were determined. Estimated cerebral perfusion pressure was calculated according to the following equation: Estimated cerebral perfusion pressure = Mean cerebral blood flow velocity/(Mean cerebral blood flow velocity – Diastolic cerebral blood flow velocity) × (Mean blood pressure – Diastolic blood pressure). Because the diameters of the vessels could not be measured directly, an index of resistance was calculated according to the following equation: Resistance area product = Mean blood pressure/Mean cerebral blood flow velocity. We calculated an index of cerebral blood flow according to the following equation: Index = Estimated cerebral perfusion pressure/Resistance area product. Patients were reassessed at 24 and 48 hours after delivery. Results: At the initial assessment the estimated cerebral perfusion pressure was higher in women with eclampsia than in those with severe preeclampsia. In addition, cerebrovascular resistance was significantly decreased in the eclampsia group, and it remained decreased as long as 4 days in 1 patient with eclampsia. Conclusions: Preeclampsia is associated with increases in cerebral perfusion pressure counterbalanced by increases in cerebrovascular resistance, with no change in cerebral blood flow. In eclampsia a significant increase in cerebral perfusion pressure occurs, but a significant fall in cerebrovascular resistance also occurs and a loss of autoregulation results in cerebral overperfusion similar to that of hypertensive encephalopathy. This may persist for as long as 4 days. (Am J Obstet Gynecol 1999;181:1162-5.)

Response of cerebral blood flow and cerebrovascular reactivity to acetazolamide in patients with dementia and idiopathic normal-pressure hydrocephalus

The responses of cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to administration of acetazolamide were investigated in 16 patients with dementia and ventriculomegaly to clarify the cerebral hemodynamics in patients with idiopathic normal-pressure hydrocephalus (NPH). The mean CBF velocity in the whole brain was measured by the Patlak plot method by using technetium-99m hexamethylpropyleneamine oxime single-photon emission computerized tomography. The CVR values were obtained from the response to administration of 500 mg of acetazolamide and calculated as the percentage of change from the baseline mean CBF value. The mean CBF value was significantly reduced (p &lt; 0.01) in six patients with (35.2 ± 5 ml/100 g/minute) and 10 patients without (33.5 ± 2.8 ml/100 g/minute) NPH compared with the age-matched normal controls (40.8 ± 3.2 ml/100 g/minute), showing no significant difference. The CVR was significantly impaired in patients with NPH (0.8 ± 1.7%; p &lt; 0.001), whereas in patients without NPH preserved CVR (11.3 ± 3%) was demonstrated compared with the normal controls (14.7 ± 1.1%). In patients with NPH a significantly lower CVR (p &lt; 0.001) was shown than in those without NPH. The CVR significantly increased (p &lt; 0.001) after placement of a shunt in patients with NPH. Reductions in both CBF and CVR may be diagnostic indicators of NPH in patients with dementia in whom ventriculomegaly is present. In patients with dementia and idiopathic NPH both reduced CBF and extremely impaired CVR are shown. The results of the present study suggest that ischemia due to the process of NPH is responsible for the reduction of CBF and manifestation of symptoms in patients with idiopathic NPH.

Effect of CO2 on dynamic cerebral autoregulation measurement

Arterial pCO2 is known to influence cerebral autoregulation but its effect on the dynamic relationship between mean arterial blood pressure (ABP) and mean cerebral blood flow velocity (CBFV), obtained from spontaneous fluctuations in ABP, has not been established. In 16 normal subjects, ABP was measured non-invasively (Finapres), CBFV was estimated with Doppler ultrasound in the middle cerebral artery, and end-tidal CO2 (EtCO2) was measured with an infrared capnograph. Recordings were made before, during and after breathing a mixture of 5% CO2 in air. The coherence function, amplitude and phase frequency responses, and impulse and step responses for the effects of ABP on CBFV were calculated by spectral analysis of beat-to-beat changes in mean ABP and CBFV before (mean CO2 5.55±0.38 kPa), during (6.43±0.31 kPa) and after 5% CO2 (5.43±0.26 kPa). During 5% CO2, the coherence function and the amplitude frequency response were significantly increased for frequencies below 0.05 Hz and the phase was reduced for the frequency range 0.02 - 0.1 Hz. The impulse and step responses indicated that 5% CO2 reduces the efficiency of the autoregulatory mechanism. A 20.7% average increase in CBFV induced by a 14.4% increase in EtCO2 was found to be mediated by a 25.9% reduction in critical closing pressure, while the change in resistance-area product was non-significant.

Cerebral blood flow velocity during tilt table test for pediatric syncope.

Brain hypoperfusion during neurocardiogenic syncope develops as a consequence of hypotension and bradycardia. Transcranial Doppler indicates that an increase in cerebral vascular resistance occurs before or during the loss of consciousness. Cerebral blood flow velocity was studied during tilt table testing in pediatric patients with neurocardiogenic syncope. We assessed whether a critical reduction in flow velocity (>40%) was predictive of the presyncopal manifestations during the test. A 2-MHz transcranial Doppler measured blood flow velocity in the right middle cerebral artery in 27 pediatric patients (ages, 8 to 18 years) during a three-stage 80 degrees tilt table test protocol. A positive test required development of syncope or presyncope with at least 30% decrease in systolic blood pressure and/or heart rate relative to preceding values. Patients were divided into: group I (isoproterenol-induced positive tests), group II (positive without isoproterenol), and group III (negative tests). Within the first 3 minutes of the upright position mean cerebral blood flow velocity in groups I, II, and III decreased by 18%, 29%, and 17%, respectively, as the systolic and diastolic blood pressures showed only minimal changes. A decreased mean blood flow velocity of 48% and 45% and an increase in resistance index of 42% and 26% from supine values in the absence of hypotension, were detected in groups I and II at 46 seconds (range, 30-120 seconds) and 50 seconds (range, 0-300 seconds) before any clinical symptom (presyncope latency). Mean blood flow velocity during presyncope decreased by 58% and 59%, whereas resistance index was double. A significant correlation (rho = -0.62) was found between presyncope latency and the decreased mean cerebral blood flow velocity. Similar blood flow velocity changes were not detected in group III. A sustained reduction >40% in mean cerebral blood flow velocity in the absence of hypotension always resulted in presyncopal or syncopal manifestations. It seems that once this critical threshold is identified during the tilt table testing, supine position may be resumed several seconds before the clinical manifestations of syncope.

Administration of hypertonic (3%) sodium chloride/acetate in hyponatremic patients with symptomatic vasospasm following subarachnoid hemorrhage.

A retrospective study was carried out to evaluate the effect of hypertonic (3%) saline chloride/acetate on various hemodynamic parameters in mildly hyponatremic patients with symptomatic vasospasm following aneurysmal subarachnoid hemorrhage (SAH). We identified 29 hyponatremic (serum sodium < 135 mEq/L) patients who received hypertonic (3%) sodium chloride/acetate as a continuous infusion. Administration of hypertonic (3%) sodium chloride/acetate resulted in higher central venous pressures and positive fluid balance, with a concomitant increase in serum sodium and chloride concentrations without metabolic acidosis. There were no changes in mean cerebral blood flow velocities after infusion of hypertonic (3%) sodium chloride/acetate. We found no reports of congestive heart failure, pulmonary edema, metabolic acidosis, coagulopathy, intracranial hemorrhages, or central pontine myelinolysis in any of these patients. We conclude that hypertonic (3%) sodium chloride/acetate can be administered to patients with mild hyponatremia in the setting of symptomatic vasospasm following SAH without untoward effects. Sample size and limitations of a retrospective analysis preclude conclusions about safety and efficacy of hypertonic (3%) sodium chloride/acetate administration in this patient population. However, our results support justification for a prospective, randomized, double-blind trial of hypertonic (3%) sodium chloride/acetate versus normal saline in patients with symptomatic vasospasm following SAH.

Transcranial Doppler sonography during acute 80° head-down tilt (HOT) for the assessment of cerebral autoregulation in humans

Cerebrovascular hemodynamics during postural changes have been sparsely Investigated despite the fact that abnormal responses may contribute to the risk of stroke. The aim of this study was to determine the effect of acute 80° head-down tilt (HDT) on cerebrovascular hemodynamics in humans using transcranial Doppler sonography (TCD). In 13 healthy volunteers (2 female, 7 1 male, age 19-37 years, mean age 26.8 years) left midcerebral artery blood flow velocities (CBFVs) were continuously monitored using TCD during 180 sec in horizontal position and during 60 sec of 80° HDT. Simultaneously, systolic, diastolic, mean CBFVs, pulsatility index (PI), heart rate, beat-to-beat blood pressure (BP) and transcutaneous pC02 were measured. In five volunteers, the procedure was repeated the next day to test the repeatability of the results. Mean BP increased slightly, but not significantly during tilt (from 80.5± 7.7 mmHg to 85.9 ±14.1 mmHg; p < 0.05). Heart rate decreased significantly during the first 20sec of HDT (from 66.8± 9.9 min-1 to 60± 11 min-1; p> 0.05). Transcutaneous pC02 was within physiological ranges during the whole procedure (mean pC02 minimum 39.5±2.9 mmHg, mean pC02 maximum 42.2±3.3 mmHg). Mean CBFV did not change significantly during tilt (from 70.1 ± 7 9.1 cm sec-1 to 66.6 ± 14.1 cm sec-1; p < 0.05). PI, however, increased significantly with a more pronounced increase during the first 20 sec than the last 40sec of tilt (Plsupine 0.92±0.11; Pltnt(0-20sec) 1.15±0.18; Pltnt(2i~6o sec) 1-03±0.16; p = 0.001; p = 0.017). The HDT results were found to be reproducible in the five volunteers. During 80°-HDT mean BP and pC02 did not change significantly. This observation combined with the significant decrease in heart rate during the first 20 sec of HDT, suggests that there is no sympathetic activation. The significant PI increase during HDT indicates a vasoconstriction of the cerebral resistance vessels. We assume that this vasoconstriction is due to the myogenic mechanism of cerebrovascular autoregulation triggered by a rapid, passive intracranial blood volume influx during HDT. [Neurol Res 1999; 21: 457–462]

Cerebrovascular mechanisms in neurocardiogenic syncope with and without postural tachycardia syndrome

Background and purpose: Recent transcranial Doppler studies in patients with neurocardiogenic syncopes (NCS) have demonstrated that the cerebrovascular response to sudden systemic hypotension is vasoconstriction instead of compensatory vasodilation (autoregulation). We tried to characterize the conditions leading to this unexpected response in NCS patients further by continuously monitoring autoregulation and autonomic parameters during a standardized tilt-table test (TTT). Methods: Sixteen patients below the age of 50 years with a history of at least three syncopes of undetermined cause and tilt-table verified NCS and 20 normal controls were studied. Arterial blood pressure (ABP) and heart rate (HR) were monitored by Finapres and cerebral blood flow velocity (CBFV) of the left middle cerebral artery by transcranial Doppler. Baroreflex sensitivity and autoregulation parameters were measured continuously, using cross-spectral analysis of Mayer waves (3–9 cycles per minute oscillations) in ABP, HR and CBFV, respectively. Pulsatility indices (PI) of CBFV and ABP were determined continuously. Measurements were taken during 5 min in supine and during 5 min in tilted position. In patients, tilting was continued for a maximum of 45 min until the onset of syncope or presyncope. Results: According to the maximum increase in heart rate (ΔHR) during the first 5 min of standing, heart rate responses were classified as postural tachycardia syndrome (POTS) (ΔHR>35/min) or as normal. Only one out of 20 control subjects showed a POTS (5%) in contrast to seven patients (44%). Patients with a POTS had significantly lower PI values in ABP and higher ratios between the PI of CBFV and the PI of ABP both in supine and in tilted positions. Baroreflex sensitivity during standing decreased significantly in POTS patients when compared to controls. Although autoregulation remained intact during standing, mean CBFV decreased significantly and continuously. The nine patients without a POTS showed almost the same cardiovascular and cerebrovascular responses as the control subjects. All 16 patients showed similar circulatory responses during syncope (sudden hypotension, relative or absolute bradycardia, reduced CBFV and increased PI in CBFV). Conclusions: The development of a POTS during tilting indicates a high risk for fainting. The characteristic hemodynamic features in the initial phase of standing in these patients can be interpreted in terms of central hypovolemia (low PI of ABP) with sufficient ABP regulation and increased cerebrovascular resistance (defined as the ratio between PI of CBFV and ABP). Cerebral autoregulation seems not to be affected in patients suffering from NCS.

Cerebral Blood Flow Velocity Changes after Bovine Natural Surfactant Instillation

OBJECTIVE: To determine the effects of bovine natural surfactant (beractant) instillation on cerebral hemodynamics in preterm infants with respiratory distress syndrome (RDS). STUDY DESIGN: Preterm infants who required surfactant for RDS were enrolled. Cerebral blood flow velocity (CBFV) waveforms from the pericallosal artery were analyzed by pulsed Doppler ultrasonography with the anterior fontanel serving as an acoustic window. CBFV was measured before and at 5, 10, 20, and 30 minutes after the first dose of a bolus instillation of surfactant in four aliquots. Simultaneously with CBFV measurements, mean blood pressure (MBP), heart rate, and ventilator settings were recorded. pH, PACO2, and PAO2 before and at 30 minutes after surfactant administration were also determined. RESULTS: The 30 enrolled preterm infants had a mean birth weight of 973 gm (513 to 1996 gm) and a mean gestational age of 27 weeks (23 to 33 weeks). Mean postnatal age at surfactant administration was 4.7 ± 2.7 hours. There were no significant changes in pH and PACO2 before and at 30 minutes after surfactant (before surfactant: mean pH of 7.29 ± 0.07 and mean PACO2 of 44.4 ± 7.1 torr; after surfactant: mean pH of 7.31 ± 0.07 and mean PACO2 of 42.7 ± 8.3 torr). PAO2 increased significantly from a pre-surfactant mean of 83 torr to 130 torr at 30 minutes after surfactant (p < 0.05), with no significant changes in mean airway pressure. There were no significant changes in MBP, heart rate, mean CBFV, peak systolic flow velocity, and diastolic flow velocity before and after surfactant instillation regardless of gestational age. Individual changes in mean CBFV were related to MBP changes (p < 0.001, linear mixed models with random effects). CONCLUSION: In low birth weight infants with RDS, bovine surfactant instillation is not associated with a significant alteration in cerebral hemodynamics. However, the direct relationship between CBFV and MBP is consistent with the reported pressure-passive cerebral circulation in sick preterm infants.

Cerebral blood flow velocity during neonatal seizures

AIMTo determine if cerebral blood flow velocity increases during all types of neonatal seizure, and whether the effect is due solely to an increase in blood pressure, transmitted to the...

Cerebral blood flow velocity and carbon dioxide vasoreactivity during γ-hydroxybutyrate/fentanyl anaesthesia in non-neurosurgical patients

In this study the effects of γ-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (JOURNAL/ejanet/04.03/00003643-199903000-00010/OV0312/v/2021-02-06T021413Z/r/image-pngmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with γ-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg−1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect JOURNAL/ejanet/04.03/00003643-199903000-00010/OV0312/v/2021-02-06T021413Z/r/image-pngmean [awake: 57±12 cm s−1 (mean ± SD); 22.5 min: 62±15 cm s−1, NS difference] or mean arterial blood pressure (MAP) (awake: 97 ± 12 mmHg; 22.5 min: 89±10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 μg kg−1 and vecuronium 0.1 mg kg−1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal PCO2 of 4.6 ± 0.4 kPa (30 min). At 30 min after the start of the GHB infusion, JOURNAL/ejanet/04.03/00003643-199903000-00010/OV0312/v/2021-02-06T021413Z/r/image-pngmean and MAP decreased to 38±10 cm s−1 and 76±12 mmHg (both P<0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal PCO2 3.5±0.2 mmHg), JOURNAL/ejanet/04.03/00003643-199903000-00010/OV0312/v/2021-02-06T021413Z/r/image-pngmean decreased to 29±7 cm s−1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in JOURNAL/ejanet/04.03/00003643-199903000-00010/OV0312/v/2021-02-06T021413Z/r/image-pngmean/0.133 kPa change in the end-tidal PCO2 from normocapnia to hypocapnia) to be estimated as 2.7±1.6% 0.133 kPa−1. This suggests that cerebrovascular response to CO2 during γ-hydroxybutyrate/fentanyl anaesthesia is maintained.

中等度低体温体外循環時のｔｒａｎｓｃｒａｎｉａｌ Ｄｏｐｐｌｅｒによる脳血管ＣＯ２反応性の評価

We have evaluated cerebral blood flow velocities (CBFV) using transcranial Doppler (TCD) during cardiovascular surgery under extracorporeal circulation. We attempted to determine cerebrovascular reactivity to CO2 pressure by varying the concentration of inspired CO2 and measuring CBFV with TCD under moderate hypothermia. In this study, 66 patients (mean age: 63.6±7.2 years) who underwent cardiac operations were assessed over a four-year period. Forty patients received aorto-coronary bypass grafts, 13 patients had valvular heart disease, and 12 had congenital septal defects. One patient had a left atrial myxoma. In all cases, cardiac surgery was performed with moderate hypothermia and non-pulsatile cardiopulmonary bypass. The pump flow was fixed at 2.6 L/min/m2 in all patients.Patients were divided into three groups according to age (cut-off value, 70 years) and type of surgery. Among the 41 patients under 70 years old, 15 patients underwent closure of septal defects or replacement of heart valves (non-CABG group), and 26 received coronary arterial bypass grafts (CABG group) . All of the 25 patients aged over 70 years received CABGs (elderly group) . As in the non-CABG group, there was a close correlation between PaCO2 and mean CBFV (mean CBFV=-2.47+1.21×PaCO2, R2=0.429) . The patients in the CABG group showed a mild linear correlation between PaCO2 and mean CBFV (mean CBFV=1.64+0.89×PaCO2, R2=0.216) . There were no significant correlations in the elderly group.It is concluded that flow velocity is increased under moderate hypothermia in proportion to increased PaCO2 in patients aged under 70 years. TCD is a practical non-invasive monitoring system and can provide an approximation of changes in cerebral circulation during moderate hypothermia.

Cerebral blood flow velocity during occlusive manipulation of patent ductus arteriosus in children.

Patent ductus arteriosus (PDA) with left-to-right shunting modifies the Doppler flow pattern of the intracranial circulation. The ability of increases in cerebral blood flow velocity (CBFV) to predict shunt resolution during PDA occlusion was evaluated. A 2 MHz transcranial Doppler (TCD) monitored diastolic and mean CBFV, plus the systolic/mean CBFV ratio in the middle cerebral artery from before (baseline) to immediately after PDA occlusion. Shunt resolution was verified by echocardiography and/or angiography. A minimum of 40% increase in diastolic-CBFV from baseline was considered successful resolution. Patients were age-stratified into group I (< 15 months; n = 23) and group II (> 15 months; n = 10). Thirty-three children were studied (age, 0.1 to 109 months) during surgical (n = 22) or coil occlusions (n = 11). Transcranial Doppler successfully identified shunt resolution in 78% of cases in group I, as compared to 0% in group II (p < 0.01). Identification rate decreased from 79% in cases of minimum ductal diameter of 3 mm (n = 19) to 21% in smaller ductuses (n = 14) (p < 0.01). Body weight and left-atrium size (p = 0.004) in group I and PDA diameter in group II (p = 0.02), were the only preoperative ductal parameters associated with diastolic-CBFV changes after ductus occlusion. Transcranial Doppler detects shunt resolution in infants with moderate to large PDAs.

Passive and active exercises increase cerebral blood flow velocity in young, healthy individuals.

Unlike the well-examined cardiovascular changes during movement stimuli, changes of cerebral hemodynamics and cerebral metabolism in physical exercises have, as yet, rarely been studied. Our objective was to investigate whether there are changes in cerebral hemodynamics and cerebral metabolism caused by active and passive movement stimuli. Response to repetitive active and passive movement stimuli was studied in 14 volunteers (8 females, 6 males; mean age, 35.2+/-8 yr). Each volunteer was subjected to four measurement series while performing a defined active and passive exercise program of the right upper or right lower limb. Measurement series were designed according to Aaslid's "evoked flow test"; exercises were performed for 20 s, followed by a rest of 20 s. This sequence was repeated 10 times in each series. As a measure of cerebral hemodynamics mean and peak blood flow velocity of the middle cerebral artery were recorded by transcranial Doppler sonography (Multidop-X-DWL). In addition, cerebral metabolism was quantified in a subsample by means of oxygenic cytochrome aa3 (respiratory chain enzyme), cerebral oxygen saturation using near infrared spectroscopy (Critikon). As well, noninvasive blood pressure (Penaz method) and expiratory pCO2 were measured. Compared with resting measures, an increase in mean cerebral blood flow velocity of the middle cerebral artery of 3.8% (P = 0.003, paired t test) was observed after active exercises of the right lower limb and 3.5% after active exercises of the right upper limb. Respective changes were 3.4% (P = 0.004) for passive exercises of the lower limb and 4.6% (P = 0.007) for passive exercises of the right upper limb. Peak cerebral blood flow velocity of the middle cerebral artery showed an even more pronounced increase during passive and active exercises in all cases, with values of between 12.2% (P < 0.001) and 13.6% (P < 0.001). Significant increases (1.5-3%) of cytochrome aa3 and cerebral oxygen saturation were observed during active and passive exercises. These studies show that active as well as passive exercises are followed by an increase of cerebral blood flow velocity. We attribute the increase of cerebral hemodynamic and cerebral metabolism to cerebral activation and autoregulative mechanisms.

Transcranial Doppler Ultrasonographic Features During Drug Withdrawal From Drug‐Induced Headache. A Transcranial Doppler Follow‐up Study

A vascular component in ergotamine-induced headache has been proposed. No study has been carried out to evaluate cerebral hemodynamic changes by means of transcranial Doppler during withdrawal from migraine medication; in particular, ergotamine-containing drugs. We examined 21 patients suffering from drug-induced headache during their in-hospital withdrawal from ergotamine (n=8) and compared them with patients during withdrawal from analgesics (n=13) and with healthy controls (n=14). Cerebral blood flow velocities were measured with transcranial Doppler, and pulsatility indices were calculated. Blood pressure, heart rate, and end-tidal carbon dioxide were documented. A subjective analog headache rating scaling was used for day-to-day evaluation of headache severity. Mean cerebral blood flow velocities dropped significantly after discontinuation of ergotamine-containing drugs but not after stopping common analgesics. Pulsatility indices remained unchanged. Cerebral blood flow velocities were higher in drug-ingesting patients compared to the control group and showed significant changes in patients with headache using ergotamine and in those using analgesics. Carbon dioxide, heart rate, and blood pressure remained unchanged. The headache rating scale did not show a constant trend. Our results indicate that ergotamine and, to a lesser extent, common analgesics including caffeine might influence cerebral blood flow velocities and pulsatility indices causing transient and reversible disturbance of cerebral autoregulation.

The effect of phototherapy on cerebral blood flow velocity in preterm infants

Cerebral blood flow velocity was studied with two‐dimensional/pulsed Doppler ultrasound before, during and after discontinuation of phototherapy in 22 preterm infants (gestational age ≤ 32 weeks), who were treated for a minimum of 12 h with blue‐light phototherapy for non‐haemolytic hyperbilirubinaemia. Before the cerebral blood flow velocity measurements, patency of the ductus arteriosus was diagnosed by Doppler echocardiography. All infants had normal brain ultrasound scans. Mean cerebral blood flow velocity increased significantly after initiation of phototherapy in all infants. Only in “healthy” (non‐ventilated) infants did cerebral blood flow velocity return to pre‐phototherapy values (baseline) after discontinuation of phototherapy, whereas in “unhealthy” (ventilated) infants cerebral blood flow velocity did not return to baseline. In 10 infants the ductus arteriosus reopened during phototherapy. In those infants, mean cerebral blood flow velocity returned to pre‐phototherapy values after 2 h of phototherapy prior to its discontinuation.

Effect of nitrous oxide on cerebral blood flow velocity after induction of hypocapnia.

Hyperventilation may reverse increases in cerebral blood flow velocity caused by inhalation of nitrous oxide (N2O). This study sought to determine whether inhalation of 50% nitrous oxide after the induction of hyperventilation increases cerebral blood flow velocity as measured by transcranial Doppler ultrasonography. Seven volunteers breathed air/O2 through a modified Circle system at normocapnia followed by air/O2 with hyperventilation, and then N2O/O2 with hyperventilation. Expired gas concentrations were measured in the expiratory limb of the circuit distal to a one-way valve. Hyperventilation reduced end-tidal carbon dioxide from 38+/-1 mmHg to 26+/-1 mmHg. Hypocapnia was maintained during inhalation of N2O (EtCO2=28+/-1 mmHg). Mean cerebral blood flow velocity decreased 34% with hyperventilation (38+/-4 cm/second versus 59+/-9 cm/second, p < 0.05) and returned to baseline with the addition of nitrous oxide (58+/-7 cm/second), despite persistent hypocapnia. The addition of nitrous oxide to the inspired gas mixture after induction of hypocapnia reversed reductions in cerebral blood flow velocity associated with hyperventilation. Potential benefits of induced hypocapnia in patients with intracranial pathology may be offset by the administration of N2O.