Abstract 15284: Characteristics and Determinants of Cerebral Circulation in Patients after Surgery for Congenital Heart Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hirofumi Saiki ◽  
Seiko Kuwata ◽  
Clara Kurishima ◽  
Yoichi Iwamoto ◽  
Hirotaka Ishido ◽  
...  

Background: Neurodevelopmental delay and cerebral atrophy coupled with reduced blood flow are reportedly closely linked in patients with congenital heart diseases (CHD). However, the mechanisms to regulate cerebral flow in the same are unclear. Cardiac output and underlying cerebral arterial resistance that is constructed during infancy may affect blood perfusion. We tested our hypothesis that cerebral blood flow in patients with repaired CHD is affected by the original features of CHD. Method: Ninety children including 50 patients with biventricular repaired CHD (ToF 27, TGA 15, CoA+VSD 8), 15 with a single ventricle (SV: Glenn7/Fontan8) and 25 with negligible shunts and otherwise normal stracture heart were enrolled. During cardiac catheterization, cardiac index (CI), blood pressure, central venous pressure were measured before and after inferior vena cava occlusion. Assuming that cerebral resistance (Rc) and lower body resistance (Ri) are constant during IVC occlusion, the resistance and blood distribution to the brain and lower body were calculated as a parallel resistance circuit. The impacts of hemodynamics on the cerebral circulation were analyzed. Result: The cerebral portion of cardiac index (CIc) was negatively correlated with age (CIc=1.88-0.06*Age, p<.05) and positively correlated with the CI (CIc=0.26+0.35*CI, p<.0001). As expected, the cerebral resistance (Rc) increased significantly with age (p<.05), whereas the resistance ratio defined as the Rc/Ri was independent of age, body size, disease, and surgical history. Multivariate analysis revealed that the CI was the independent determinant of CIc, regardless of the underlying diseases (p<.01, β=0.27). Interestingly, after adjusting for age and CI, repaired CoA exhibited significantly higher Rs/Ri ratio (p<.01) and lower CIc (p<.05) than other groups, whereas SV patients showed significantly increased CIc, CIc/CI ratio and lower Rc compared to other groups (p<.05). Conclusion: Apart from the strong governance of cerebral blood flow by cardiac output, cardiovascular property before anatomical repair and cavo-pulmonary connections have a significant impact on the cerebral circulation. Long-term effects of abnormal cerebral circulation warrants further studies.

Neurosurgery ◽  
2003 ◽  
Vol 53 (5) ◽  
pp. 1044-1052 ◽  
Author(s):  
Dong H. Kim ◽  
Mathew Joseph ◽  
Saleem Ziadi ◽  
Joseph Nates ◽  
Mark Dannenbaum ◽  
...  

Abstract INTRODUCTION Vasospasm after subarachnoid hemorrhage remains a management challenge. The accepted treatment involves hypertensive, hypervolemic, hemodilution therapy. However, there is variation in the application of this treatment. Most authors increase mean arterial pressure (MAP), which can be associated with significant morbidity. Others increase cardiac output (CO). In this study, we examined the relationship between volume status, CO, and MAP and cerebral blood flow (CBF) in the setting of vasospasm. METHODS A xenon blood flow tomography-based system was used to quantitate CBF. Sixteen patients with vasospasm after subarachnoid hemorrhage were treated with hypervolemia, phenylephrine to increase MAP, or dobutamine to increase CO. Direct CBF measurements were obtained before and after treatment. A strength of this study is that only one variable (central venous pressure, MAP, or CO) was manipulated in each patient, and the effect of this change was measured immediately. RESULTS With phenylephrine, mean MAP increased from 102.4 to 132.1 mm Hg. In regions of diminished CBF due to vasospasm, mean CBF increased from 19.2 to 33.7 ml/100 g/min. Similarly, dobutamine increased the cardiac index from a mean of 4.1 to 6.0 L/min/m2 and slightly decreased MAP. CBF increased from a mean of 24.8 to 35.4 ml/100 g/min. Both were statistically significant changes. With hypervolemia, the average central venous pressure increased from a mean of 5.4 to 7.3 cm H2O; no changes in mean CBF were noted. CONCLUSION This article reports the first human study that shows with direct measurements the independent influence of CO in the setting of vasospasm. Increases in CO without changes in MAP can elevate CBF. This finding has immediate clinical application because CO manipulation is much safer than increasing MAP. Because both interventions were equally efficacious, our protocol has been changed to augment CO as a first measure. Induced hypertension is reserved for patients in whom this initial treatment fails.


1980 ◽  
Vol 48 (3) ◽  
pp. 468-472 ◽  
Author(s):  
F. A. Leahy ◽  
D. Cates ◽  
M. MacCallum ◽  
H. Rigatto

To determine 1) the effect of arterial CO2 change on the neonatal cerebral circulation and 2) whether 100% O2 would produce significant decrease in cerebral blood flow (CBF), we studied 24 preterm infants to explain the late (5 min) hyperventilation observed in them during hyperoxia. Of these, 12 were studied before and during inhalation of 2-3% CO2 and 12 before and during the inhalation of 100% O2. We measured CBF by a modification of the venous occlusion plethysmography technique and found that CBF increased 7.8% per Torr alveolar carbon dioxide pressure change and that it decreased 15% with 100% O2. These findings suggest that 1) CO2 is an important regulator of CBF in the perterm infant, 2) CBF-CO2 sensitivity in these infants may be greater than in adult subjects, 3) 100% O2 reduced CBF significantly, and 4) a decrease in CBF during administration of 100% O2 may be at least partially responsible for the increase in ventilation with hyperoxia.


1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
AM Harper

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.


1982 ◽  
Vol 62 (2) ◽  
pp. 17P-17P ◽  
Author(s):  
P.J. Cook ◽  
C.G. Maidment ◽  
I.M. James ◽  
R.A. Hutton ◽  
P. Dandona

1989 ◽  
Vol 256 (3) ◽  
pp. H779-H788
Author(s):  
R. C. Koehler ◽  
J. E. Backofen ◽  
R. W. McPherson ◽  
M. D. Jones ◽  
M. C. Rogers ◽  
...  

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Amulya Buddhavarapu ◽  
Luisa Raga ◽  
Euleche Alanmanou ◽  
Prashob Porayette

Introduction: Cardiac magnetic resonance imaging (CMR) can reliably assess hemodynamics in children. Anesthetic agents may affect cerebral blood flow (CBF) and change the cerebral to systemic perfusion ratio. Hypothesis: Volatile anesthetic agents cause significant cerebral vasodilation resulting in descending aorta (DAo) flow reversal. Methods: Blood flow was measured in patients who underwent cine phase contract velocity mapping during CMR (1.5T, Philips Ingenia, Amsterdam, The Netherlands) with or without general anesthesia (GA) at our institution. Patients with a known cause for flow reversal in DAo (e.g. aortic insufficiency, aorto-pulmonary shunt/collaterals) or brain pathology were excluded. Flows in superior vena cava (SVC, surrogate for CBF), ascending aorta (AAo, measure of cardiac output), and DAo (measure of lower body perfusion) were analyzed. Measures of central tendency, standard deviation, correlation coefficient and Student’s t-test were calculated. Variables including anesthetic agents, body surface area (BSA), mechanical ventilator parameters and vital signs were assessed. Results: A total of 93 CMR scans were performed with GA (n=43, age 3 m to 15 y, BSA 0.29-2.4 m 2 ) or without GA (n=50, 2 w to 21 y, BSA 0.2-2.89 m 2 ). There was significant flow reversal in DAo (mean 7.62% +/- SD 7%) in GA group using volatile agents compared to non-GA patients (1.16% +/- 1.78%; p-value <0.001). SVC flow was higher in GA (1.66+/-1.02 ml/min/m 2 ) than non-GA patients (1.28+/-0.53 ml/min/m 2 ) but did not reach statistical significance (p=0.06). GA group had significantly higher SVC (cerebral blood) to AAo flow (cardiac output) ratio (0.53 +/- 0.13) than non-GA group (0.44 +/- 0.17; p=0.003), probably from increased CBF from cerebral vasodilation by volatile anesthetic agents. Patients with BSA >1.2 m 2 and GA (0.84 +/- 0.27) had a tendency to have higher SVC/DAo flow ratio compared to non-GA (0.69 +/- 0.3; p = 0.06) patients. There was a positive correlation between the end tidal CO 2 and SVC flow (r 0.486, R 2 0.236). Conclusions: The flow rates of SVC, AAo and DAo using CMR must be interpreted with caution in children, taking into account the effects of GA on the cerebral and lower body perfusion. This difference may be relevant in patients with congenital heart disease, especially with cavo-pulmonary and Fontan circulation.


1994 ◽  
Vol 266 (2) ◽  
pp. H458-H467 ◽  
Author(s):  
J. N. Brown ◽  
A. L. Nuttall

Autoregulation of blood flow in the inner ear following uncontrolled changes in systemic blood pressure (BP), which was induced by the application of pharmacological agents that cause local and/or systemic vascular effects, has been reported in previous studies. In the current study, carotid BP was systematically manipulated without drugs, while the resulting cochlear blood flow (CBF) changes were measured using a laser Doppler flowmeter (LDF). Anesthesized guinea pigs were used, and the probe of a LDF was held against the ventral-posterior portion of the surgically exposed cochlea. A mechanical occluder was placed around the descending aorta or the inferior vena cava. BP could be elevated or lowered over a wide range and was held stable during 2-min occlusions. The mean level (+/- SD) of regulation (% delta CBF/% delta BP) for BP changes less than +/- 35% of preocclusion baseline was 0.24 +/- 0.2 (or 0.18 +/- 0.2 if BP is corrected by subtracting central venous pressure). Significant regulation occurred for BP between 20 and 70 mmHg. A demonstration of the cochlear origin of the regulatory response was obtained by “pharmacological blockade” following topical application of the vasodilator, sodium nitroprusside, to the cochlea. In this condition, CBF changed in nearly direct proportion to BP.


2018 ◽  
Vol 6 (4) ◽  
pp. e13594 ◽  
Author(s):  
Noud van Helmond ◽  
Blair D. Johnson ◽  
Walter W. Holbein ◽  
Humphrey G. Petersen-Jones ◽  
Ronée E. Harvey ◽  
...  

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