scholarly journals Cerebral Blood Flow Monitoring in High-Risk Fetal and Neonatal Populations

2022 ◽  
Vol 9 ◽  
Author(s):  
Rachel L. Leon ◽  
Eric B. Ortigoza ◽  
Noorjahan Ali ◽  
Dimitrios Angelis ◽  
Joshua S. Wolovits ◽  
...  

Cerebrovascular pressure autoregulation promotes stable cerebral blood flow (CBF) across a range of arterial blood pressures. Cerebral autoregulation (CA) is a developmental process that reaches maturity around term gestation and can be monitored prenatally with both Doppler ultrasound and magnetic resonance imaging (MRI) techniques. Postnatally, there are key advantages and limitations to assessing CA with Doppler ultrasound, MRI, and near-infrared spectroscopy. Here we review these CBF monitoring techniques as well as their application to both fetal and neonatal populations at risk of perturbations in CBF. Specifically, we discuss CBF monitoring in fetuses with intrauterine growth restriction, anemia, congenital heart disease, neonates born preterm and those with hypoxic-ischemic encephalopathy. We conclude the review with insights into the future directions in this field with an emphasis on collaborative science and precision medicine approaches.

PEDIATRICS ◽  
1990 ◽  
Vol 85 (5) ◽  
pp. 733-736
Author(s):  
Margot van de Bor ◽  
Frans J. Walther ◽  
Maureen E. Sims

The pharmacologic effects of cocaine are considered to be secondary to an enhancement of the effects of circulating catecholamines. The effect of intrauterine cocaine exposure on the cerebral blood flow velocity was studied in 20 full-term newborn infants whose urine screens were positive for cocaine and in 18 nonexposed healthy full-term newborn infants whose urine screens were negative for cocaine metabolites. On the first day of life, peak systolic, end diastolic, and mean flow velocities in the pericallosal, internal carotid, and basilar arteries and mean arterial blood pressures were significantly greater in infants who had been exposed to cocaine. On day 2, cerebral blood flow velocities and mean arterial blood pressures were similar in exposed and nonexposed infants. The increase in mean arterial blood pressure and in cerebral blood flow velocity on the first day of life indicates a hemodynamic effect of cocaine that may put the infant exposed to cocaine at a greater risk of intracranial hemorrhage.


2015 ◽  
Vol 61 (6) ◽  
pp. 23S
Author(s):  
Avner B. Bar Dayan ◽  
Yefim Rabinovich ◽  
Alexander Chaikov ◽  
Otto William Brown ◽  
Yehuda G.G. Wolf

1987 ◽  
Vol 65 (1) ◽  
pp. 92-95 ◽  
Author(s):  
Cara J. MacIntyre ◽  
Bill Y. Ong ◽  
Daniel S. Sitar

Ethanol exposure in the neonatal period causes impaired brain growth and altered adult behaviour in rats. One possible mechanism may be altered cerebral perfusion caused by ethanol intoxication. We assessed the effects of ethanol on cerebral blood flow and its autoregulation in 2-day-old piglets. Piglets received ethanol (1.4 g/kg) or an equivalent volume of dextrose 5% in water over 30 min. One hour later, cerebral blood flow was measured using the microsphere technique at resting, elevated, and decreased mean arterial blood pressure. Ethanol-treated piglets had total cerebral blood flows of 88 ± 14, 82 ± 10, and 82 ± 12 mL∙100 g−1∙min−1 (mean ± SE) at mean arterial blood pressures of 12.4 ± 1.1, 15.7 ± 1.5, and 8.2 ± 0.9 kPa. Corresponding values in control piglets were 82 ± 14, 78 ± 4, and 82 ± 7 mL∙100 g−1∙min−1 at mean arterial blood pressures of 10.5 ± 1.5, 14.0 ± 1.2, and 7.7 ± 1.1 kPa. At resting arterial blood pressures, regional blood flows to basal ganglia, cortex, brainstem, and cerebellum in ethanol-treated piglets were 123 ± 21, 90 ± 16, 94 ± 17, and 77 ± 12 mL∙100 g−1∙min−1, respectively. Corresponding regional blood flows for the control piglets were 118 ± 16, 85 ± 15, 76 ± 16, and 76 ± 16 mL∙100 g−1∙min−1. Blood flow to basal ganglia was greater than to other brain regions in both ethanol-treated and control piglets (P < 0.01). Total and regional blood flows remained unchanged with altered mean arterial blood pressures, indicating normal autoregulation of cerebral blood flow in both ethanol-treated and control piglets.


1986 ◽  
Vol 64 (7) ◽  
pp. 1023-1026 ◽  
Author(s):  
B. Y. Ong ◽  
C. MacIntyre ◽  
D. Bose ◽  
R. J. Palahniuk

The cerebral blood flow of newborn lambs at reduced and elevated arterial blood pressures, induced by intravenous infusion of sodium nitroprusside and phenylephrine hydrochloride as well as blood withdrawal and reinfusion, were compared. Both blood withdrawal and sodium nitroprusside infusion reduced mean arterial pressure from 83 to 60 mmHg (1 mmHg = 133 Pa). Reinfusion of blood increased arterial pressure to 94 mmHg. Phenylephrine hydrochloride infusion increased arterial pressure to 102 mmHg. The cerebral blood flows at corresponding arterial pressures were similar (coefficient of correlation = 0.88, P < 0.01). Cerebral blood flow before and after infusion of phenylephrine hydrochloride and sodium nitroprusside into the brain via the carotid artery did not change. The results indicate that blood-borne phenylephrine hydrochloride and sodium nitroprusside, in concentrations that would alter arterial blood pressure significantly from its resting level, do not change cerebral blood flow directly.


1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.


2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.


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 ◽  
...  

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.


2018 ◽  
pp. 1-6

Background: Hypocapnia is suggested in decreasing pulmonary vascular resistance in cyanotic congenital heart disease patients undergoing definitive repair. But its effects on cerebral and renal circulation are unclear. Hence the effect of changes in arterial blood carbon dioxide tensions (PaCo2 ) on cerebral (ScO2 %) and renal (SsO2 %) oxygenation indices using Near Infrared spectroscopy (NIRS) is examined. Methods: We did a prospective observational study in sixty-eight children who underwent elective cardiac surgery for various cyanotic congenital heart diseases. PaCo2 , ScO2 % and SsO2 % were obtained before induction of anesthesia, after anesthesia induction at normocapnic or mild hypercapnic ventilation (EtCo2 =40 mmHg) and again at hypocapnic ventilation (EtCo2 =30 mmHg). Regression analysis was done between PaCo2 and NIRS-C/ScO2 % and PaCo2 and NIRS-R/SsO2 % at both EtCo2 40 and 30 mmHg. Repeated measure analysis performed to evaluate the significance of change in NIRS-C and NIRS-R from pre-anesthesia induction to when EtCo2 was 40 and then 30 mmHg post anesthesia induction. Results: With decrease in EtCo2 , PaCo2 (p=0.0001), NIRS-C (p=0.0001) and NIRS-R (p=0.0001) decreased significantly. At EtCo2 of 40 and 30 mmHg, PaCo2 had significant positive correlation with NIRS-C (R2 =0.77, p=0.0001 and R2 =0.92, p=0.0001 respectively) and had insignificant correlation with NIRS-R (R2 =0.03, p=0.12 and R2 =0.008, p=0.46 respectively). Significant changes in NIRS-C {p=0.0001} and NIRS-R {p=0.0001} occurred from pre-induction to when EtCo2 was 40 and then to 30 mmHg. Conclusion: A decrease in NIRS-C and NIRS-R is probably from decreased cerebral and splanchnic blood flow during hypocapnic ventilation, leading to demand supply mismatch. Hypocapnic ventilation in cyanotic children has potential to cause cerebral hypoxia. Abbreviations: CCHD: Cyanotic Congenital Heart Disease; QP: Pulmonary blood flow; Do2 : Oxygen delivery; SpO2 : peripheral pulse oximetry; NIRS: Near Infrared Spectroscopy; NIRS-C/ScO2 %: Regional Cerebral Oxygen saturation; NIRS-R/SsO2 %: Regional Somatic/renal Oxygen saturation; HCT: Hematocrit; ECG: Electrocardiography; CPB: cardiopulmonary bypass; TOF: Tetralogy of fallot; BDG: Bidirectional Glenn Shunt; BT shunt: Blalock Taussig shunt; DORV: Double outlet right ventricle; FiO2 : Inspired oxygen concentration; ABG: Arterial blood gas; PaO2 : Arterial oxygen partial pressure; PaCo2 : Arterial carbon dioxide partial pressure; HR: Heart rate; MAP: Mean Arterial Pressure; CVP: Central Venous Pressure


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