Simultaneous Influence of Blood Pressure, Pco2, and Po2 on Cerebral Blood Flow Velocity in Preterm Infants of Less than 33 Weeks' Gestation

Menke, Jan; Michel, Erik; Rabe, Heike; Bresser, B.; Grohs, B.; Schmitt, Rita; Jorch, G

doi:10.1203/00006450-199308000-00014

Cited by 50 publications

(42 citation statements)

References 12 publications

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“…This is in contrast to the work of others, where the lower confidence interval includes zero (13,27,28). Some authors (13) have concluded that autoregulation is preserved when the lower confidence limit encompasses zero.…”

Section: Others Have Used Doppler Ultrasound To Measure Cbfv (26 -29)contrasting

confidence: 61%

“…While the CBF still accommodates to changes in CO 2 , the magnitude of change is less than that seen by others. The infants presented here are of a lower gestational age than those studied previously (12,13,19,28,32), which may part way explain the low CO 2 -CBF reactivity. This discrepancy may be due to maturational differences in the reactivity of the CBF to acute changes in CO 2 (34).…”

Section: Others Have Used Doppler Ultrasound To Measure Cbfv (26 -29)mentioning

confidence: 49%

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CBF Reactivity in Hypotensive and Normotensive Preterm Infants

2003

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Perinatal distress in the preterm neonate, and the consequent loss of cerebrovascular autoregulation, has been implicated in the pathogenesis of neonatal cerebral lesions. A component of this distress is thought to be hypotension. We examined the autoregulatory capacity of hypotensive and normotensive infants using the 133 Xe technique to measure cerebral blood flow. Global CBF was measured during only normotension in 5 infants, and during both hypotension and normotension in 11 infants. All the infants were ventilated and blood pressure was measured using an intra-arterial catheter. Fourteen CBF measurements were made on the normotensive infants. Forty-seven CBF measurements were made on the hypotensive infants, 34 measurements during hypotension and 13 during normotension. The global CBF of the normotensive and hypotensive infants were 13.3 and 13.6 mL/ 100 g/min, respectively. The mean arterial blood pressure (MABP)-CBF reactivity (95% CI) of the normotensive and hypotensive infants were 1.9% (Ϫ0.8% to 4.7%)/mm Hg and 1.9% (0.8% to 3.0%)/mm Hg, respectively. The CO 2 -CBF reactivity (95%CI) of the normotensive and hypotensive infants was 11.1% (6.8% to 15.5%)/KPa ⌬PaCO 2 and 4.1% (Ϫ5.0% to 14.1%)/KPa ⌬PaCO 2 . The implications of these calculated CBF reactivities is that normotensive infants may have intact autoregulation but with a diminished response to fluctuations in PaCO 2 . Hypotension in the sick preterm infant has been implicated as one causative factor in the pathogenesis of a number of serious conditions including intraventricular hemorrhage (IVH) (1), periventricular leukomalacia (PVL) (2), necrotizing enterocolitis (3), and developmental delay in preterm infants (4).It is thought that perinatal asphyxia combined with hypotension leads to a loss of cerebrovascular autoregulation, which may lead to a pressure passive cerebral circulation (5). In this state, abrupt elevations in systemic blood pressure may be transmitted to the fragile vessels of the germinal matrix, possibly resulting in intraventricular hemorrhage. Historically, systemic hypotension was thought to lead to under perfusion of watershed areas, which then underwent infarction and cystic necrosis, resulting in PVL (6). Thus, absent autoregulation may be central to many causes of perinatal CNS pathology.The work of Tyszczuk et al. among others, has led to the re-evaluation of the absent autoregulation hypothesis (7). They found no significant difference between the cerebral blood flow (CBF) of normotensive infants and that of hypotensive infants. Furthermore, a number of studies have found no association between hypotension and PVL (2, 8, 9). More recently, it was found that 53% of ventilated preterm infants had evidence of impaired autoregulation (10) and Boylan et al. have identified abnormalities in the autoregulatory capacity of preterm infants (11). Only in the work of Tyszczuk was the influence of hypotension analyzed in the etiology of impaired autoregulation.Changes in arterial carbon dioxide are a major mediator of CBF variatio...

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Section: Others Have Used Doppler Ultrasound To Measure Cbfv (26 -29)contrasting

confidence: 61%

Section: Others Have Used Doppler Ultrasound To Measure Cbfv (26 -29)mentioning

confidence: 49%

CBF Reactivity in Hypotensive and Normotensive Preterm Infants

2003

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“…In addition to arbitrarily defining a critical value between 0.5 and 1.5% change in mCBFv/1 mm Hg change in MABP as intact autoregulation (30 -32), they did not take into account simultaneous changes in PaCO 2 that clearly cause changes in CBF and MABP in the same direction, which may be interpreted as impaired autoregulation. Although these critical values are somewhat arbitrary, values as high as 2.7-4% were present in infants with severe IVH, and presumably represented impaired autoregulation (14,32). We do not report a critical value inasmuch as we do not have enough study infants with severe brain injury to define a specific value.…”

Section: Discussionmentioning

confidence: 90%

The Effects of Hypercapnia on Cerebral Autoregulation in Ventilated Very Low Birth Weight Infants

2005

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Permissive hypercapnia, a strategy allowing high PaCO 2 , is widely used by neonatologists to minimize lung damage in ventilated very low birth weight (VLBW) infants. While hypercapnia increases cerebral blood flow (CBF), its effects on cerebral autoregulation of VLBW infants are unknown. Monitoring of mean CBF velocity (mCBFv), PaCO 2 , and mean arterial blood pressure (MABP) from 43 ventilated VLBW infants during the first week of life was performed during and after 117 tracheal suctioning procedures. Autoregulation status was determined during tracheal suctioning because it perturbs cerebral and systemic hemodynamics. The slope of the relationship between mCBFv and MABP was estimated when PaCO 2 was fixed at 30, 35, 40, 45, 50, 55, and Neonatologists frequently use permissive hypercapnia, a strategy that allows high PaCO 2 (45-55 mm Hg), to avoid ventilator-induced lung injury during mechanical ventilation of premature infants (1). The theoretical benefit of permissive hypercapnia is that lower tidal volumes and mean airway pressures may prevent alveolar overdistension and lung injury (1). Randomized controlled trials of permissive hypercapnia, however, failed to demonstrate significant improvements in survival without chronic lung disease over routine ventilation strategies (1,2). Despite its widespread use, the effects of permissive hypercapnia on cerebral autoregulation of premature infants are not known.Cerebral autoregulation is an essential physiologic mechanism that maintains constant blood flow to the brain despite variations in cerebral perfusion pressure (3). The BP range over which CBF remains constant is known as the autoregulatory plateau. In this portion of the curve, CBF is independent of BP and the slope is 0. Below the autoregulatory plateau, CBF declines; above it, CBF rises in a pressure-passive manner (Fig. 1 A) (4,5). In contrast, in impaired autoregulation, CBF linearly follows changes in BP (over all BPs), where the slope is significantly Ͼ0 (Fig. 1B) (6). Despite the widespread belief that cerebral autoregulation is impaired in sick, ventilated premature infants (6), recent evidence using continuous monitoring systems suggests that many premature infants do have intact autoregulation (7,8

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“…Finally, MLRA 13 was performed when MABP and ETCO 2 were used as independent variables and CBFV was used as the dependent variable.…”

Section: Methodsmentioning

confidence: 99%

Can Cerebrovascular Reactivity Be Assessed Without Measuring Blood Pressure in Patients With Carotid Artery Disease?

Dumville

Panerai

Lennard

et al. 1998

Stroke

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Background and Purpose-Conventional methods of assessing cerebrovascular reactivity (CVR) omit the influence of blood pressure (BP). This study demonstrates the significant influence of BP during the assessment of CVR in patients with carotid artery disease. Methods-In 56 subjects the CVR was bilaterally assessed by measurement of cerebral blood flow velocity change in response to inhalation of 5% CO 2 in air while BP was continuously monitored. Three methods of calculating the CVR were used: the conventional ratio between relative cerebral blood flow velocity and end-tidal CO 2 , simple linear regression, and multiple linear regression analysis (MLRA). The clinical significance of the difference in CVR indices was evaluated. The Bland-Altman test was applied to quantify the comparability and bias between measurements. The magnitude and significance of a change in BP during the CVR assessment were calculated in conjunction with an estimate of the velocity change attributed to the BP. The statistical significance of the data segment length on the variability and magnitude of the CVR index was computed. Results-The value of the CVR index was reduced by 20% and 6% in comparison to the conventional ratio approach when MLRA and linear regression were applied, respectively. With the use of MLRA, in 96% of cases the value of the BP coefficient was statistically significant, and in four patients the increase in velocity was primarily attributed to the increase in BP. Conclusions-The influence of BP is significant and requires consideration when the CVR index is calculated in patients with carotid artery disease. (Stroke. 1998;29:968-974.)

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Simultaneous Influence of Blood Pressure, Pco2, and Po2 on Cerebral Blood Flow Velocity in Preterm Infants of Less than 33 Weeks' Gestation

Cited by 50 publications

References 12 publications

CBF Reactivity in Hypotensive and Normotensive Preterm Infants

CBF Reactivity in Hypotensive and Normotensive Preterm Infants

The Effects of Hypercapnia on Cerebral Autoregulation in Ventilated Very Low Birth Weight Infants

Can Cerebrovascular Reactivity Be Assessed Without Measuring Blood Pressure in Patients With Carotid Artery Disease?

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