Abstract 15805: Longitudinal Changes in Univentricular Patients Pre-Bidirectional Cavopulmonary Connection and Pre-Fontan

Background: Little is known about serial changes in the physiology of single ventricle (SV) patients during staged palliation and if HLHS patients differ from the rest. Methods: We analyzed SV patients who had a combined cath with CMR at both the preBCPC and preFontan studies from 2016-2019. Flow contrast mapping used to calculate pulmonary arterial (Qpa) and venous (Qpv) flow. Systemic blood flow (Qs) calculated using [superior vena cava (SVC) flow + descending aortic flow at the level diaphragm]. Cerebral vascular resistance (CVRi) calculated using [ascending aortic pressure (AoP)-right atrial pressure (RAP)/SVC flow]. Systemic vascular resistance (SVR) calculated using [(AoP-RaP)/Qs]. Pulmonary vascular resistance (PVR) was calculated using [(mean PAP - LAP)/Qpv]. Results: 30 patients were found, 10 with HLHS. The BCPC unloaded the heart, EDVi fell from preBCPC to preFontan. From preBCPC to preFontan(Table1): PA flow fell, but was compensated by increased APC flow to keep QpQs~1, PApressure and PVRi fell. Compared to others, the HLHS patients had larger hearts (EDVi) and lower PA but higher APC flow at both preBCPC(Table2)and preFontan(Table3). By preFontan, HLHS patients had worse function: higher ESVi, lower EF. Conclusion: QpQs ~1 is maintained by increase in APC flow. HLHS hearts are larger and deteriorate progressively.

Acute and Chronic Fetal Anemia as a Result of Fetomaternal Hemorrhage

Introduction.Fetomaternal hemorrhage represents a transfer of fetal blood to the maternal circulation. Although many etiologies have been described, most causes of fetomaternal hemorrhage remain unidentified. The differentiation between acute and chronic fetomaternal hemorrhage may be accomplished antenatally and may influence perinatal management.Case.A 36-year-old gravida 6 para 3 presented at 37 and 5/7 completed gestational weeks with ultrasound findings suggestive of chronic fetal anemia such as right ventricular enlargement, diminished cerebral vascular resistance, and elevated middle cerebral artery end-diastolic velocity. On the other hand, signs of acute fetal decompensation such as deterioration of the fetal heart tracing, diminished biophysical score, decreased cord pH, and increased cord base deficit were noted. Following delivery, the neonate’s initial hemoglobin was 4.0 g/dL and the maternal KB ratio was 0.015 indicative of a significant fetomaternal hemorrhage.Discussion.One should consider FMH as part of the differential diagnosis for fetal or immediate neonatal anemia. We describe a unique case of FMH that demonstrated both acute and chronic clinical features. It is our hope that this case will assist practitioners in differentiating acute FMH that may require emergent delivery from chronic FMH which may be able to be expectantly managed.

Cerebral autoregulation dynamics in endurance-trained individuals

Aerobic fitness may be associated with reduced orthostatic tolerance. To investigate whether trained individuals have less effective regulation of cerebral vascular resistance, we studied the middle cerebral artery (MCA) mean blood velocity ( Vmean) response to a sudden drop in mean arterial pressure (MAP) after 2.5 min of leg ischemia in endurance athletes and untrained subjects (maximal O2 uptake: 69 ± 7 vs. 42 ± 5 ml O2·min−1·kg−1; n = 9 for both, means ± SE). After cuff release when seated, endurance athletes had larger drops in MAP (94 ± 6 to 62 ± 5 mmHg, −39%, vs. 99 ± 5 to 73 ± 4 mmHg, −26%) and MCA Vmean (53 ± 3 to 37 ± 2 cm/s, −30%, vs. 58 ± 3 to 43 ± 2 cm/s, −25%). The athletes also had a slower recovery to baseline of both MAP (25 ± 2 vs. 16 ± 1 s, P < 0.01) and MCA Vmean (15 ± 1 vs. 11 ± 1 s, P < 0.05). The onset of autoregulation, determined by the time point of increase in the cerebrovascular conductance index (CVCi = MCA Vmean/MAP) appeared later in the athletes (3.9 ± 0.4 vs. 2.7 ± 0.4s, P = 0.01). Spectral analysis revealed a normal MAP-to-MCA Vmean phase in both groups but ∼40% higher normalized MAP to MCA Vmean low-frequency transfer function gain in the trained subjects. No significant differences were detected in the rates of recovery of MAP and MCA Vmean and the rate of CVCi regulation (18 ± 4 vs. 24 ± 7%/s, P = 0.2). In highly trained endurance athletes, a drop in blood pressure after the release of resting leg ischemia was more pronounced than in untrained subjects and was associated with parallel changes in indexes of cerebral blood flow. Once initiated, the autoregulatory response was similar between the groups. A delayed onset of autoregulation with a larger normalized transfer gain conforms with a less effective dampening of MAP oscillations, indicating that athletes may be more prone to instances of symptomatic cerebral hypoperfusion when MAP declines.

Incorporating a parenchymal thermal diffusion cerebral blood flow probe in bedside assessment of cerebral autoregulation and vasoreactivity in patients with severe traumatic brain injury

Object Cerebral autoregulation may be altered after traumatic brain injury (TBI). Recent evidence suggests that patients' autoregulatory status following severe TBI may influence cerebral perfusion pressure management. The authors evaluated the utility of incorporating a recently upgraded parenchymal thermal diffusion probe for the measurement of cerebral blood flow (CBF) in the neurointensive care unit for assessing cerebral autoregulation and vasoreactivity at bedside. Methods The authors evaluated 20 patients with severe TBI admitted to San Francisco General Hospital who underwent advanced neuromonitoring. Patients had a parenchymal thermal diffusion probe placed for continuous bedside monitoring of local CBF (locCBF) in addition to the standard intracranial pressure and brain tissue oxygen tension (PbtO2) monitoring. The CBF probes were placed in the white matter using a separate cranial bolt. A pressure challenge, whereby mean arterial pressure (MAP) was increased by about 10 mm Hg, was performed in all patients to assess autoregulation. Cerebral CO2 vasoreactivity was assessed with a hyperventilation challenge. Local cerebral vascular resistance (locCVR) was calculated by dividing cerebral perfusion pressure by locCBF. Local cerebral vascular resistance normalized to baseline (locCVRnormalized) was also calculated for the MAP and hyperventilation challenges. Results In all cases, bedside measurement of locCBF using a cranial bolt in patients with severe TBI resulted in correct placement in the white matter with a low rate of complications. Mean locCBF decreased substantially with hyperventilation challenge (−7 ± 8 ml/100 g/min, p = 0.0002) and increased slightly with MAP challenge (1 ± 7 ml/100 g/min, p = 0.17). Measurements of locCBF following MAP and hyperventilation challenges can be used to calculate locCVR. In 83% of cases, locCVR increased during a hyperventilation challenge (mean change +3.5 ± 3.8 mm Hg/ml/100 g/min, p = 0.0002), indicating preserved cerebral CO2 vasoreactivity. In contrast, we observed a more variable response of locCVR to MAP challenge, with increased locCVR in only 53% of cases during a MAP challenge (mean change −0.17 ± 3.9 mm Hg/ml/100 g/min, p = 0.64) indicating that in many cases autoregulation was impaired following severe TBI. Conclusions Use of the Hemedex thermal diffusion probe appears to be a safe and feasible method that enables continuous monitoring of CBF at the bedside. Cerebral autoregulation and CO2 vasoreactivity can be assessed in patients with severe TBI using the CBF probe by calculating locCVR in response to MAP and hyperventilation challenges. Determining whether CVR increases or decreases with a MAP challenge (locCVRnormalized) may be a simple provocative test to determine patients' autoregulatory status following severe TBI and helping to optimize CPP management.

Cerebral blood flow is increased during controlled ovarian stimulation

Estrogen appears to enhance cerebral blood flow (CBF). An association between CBF and physiologically altered hormonal levels due to menstrual cycle, menopause, or exogenous manipulations such as ovariectomy or hormone replacement therapy has been demonstrated. The purpose of this study was to determine the association between ovarian stimulation and CBF in vivo by measuring blood flow in the internal carotid artery (ICA) after pituitary suppression and during controlled ovarian stimulation in women undergoing in vitro fertilization treatment cycles. ICA volume flows were measured by angle-independent dual-beam ultrasound Doppler in 12 women undergoing controlled ovarian stimulation. Measurements were performed after pituitary/ovarian suppression, in the late follicular phase, and at midluteal phase. Blood flow in the ICA increased by 22.2% and 32% in the late follicular and midluteal phases compared with the respective values obtained during ovarian suppression ( P < 0.0005 and P < 0.0001, respectively). There was a significant correlation between increments in estrogen levels and increments in CBF when the late follicular phase was compared with the ovarian suppression period ( r = 0.8, P < 0.001). Mean blood flow velocity significantly increased (by 15.7% and 16.9%, respectively) and cerebral vascular resistance significantly decreased (by 17.6% and 26.5%) during the late follicular and midluteal phases compared with respective measures during ovarian suppression. There was a significant correlation between an increase in estrogen levels and a decrease in cerebral vascular resistance when the late follicular phase was compared with the ovarian suppression period ( r = −0.6, P < 0.05). These changes imply sex hormone-associated intracranial vasodilation leading to increased CBF during controlled ovarian stimulation.