Cerebral Hemodynamics During the Valsalva Maneuver

Zhang, Rong; Crandall, Craig G.; Levine, Benjamin D.

doi:10.1161/01.str.0000120309.84666.ae

Cited by 85 publications

(39 citation statements)

References 17 publications

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“…It is reasonable to assume that there was no difference in intracranial pressure between hypertensive and normotensive groups because none of the participants showed symptoms of intracranial hypertension or hydrocephalus, and patients with tumors were removed from the study. Although many other studies have used this method of calculating cerebral vascular resistance, 22,23 the method needs validating in both healthy controls and patients with disease.…”

Section: Discussionmentioning

confidence: 99%

“…The method has been used in multiple studies to calculate cerebral vascular resistance. 22,23 Regional cerebral perfusion was measured from the pseudo continuous arterial spin labeling images using the standard Buxton model. 24 Cerebral vascular reactivity to hypercapnia (5% CO 2 ) was calculated as the change in total cerebral blood flow (calculated as the sum of blood flow in the internal carotid and basilar arteries, measured using phase contrast MRI) from the normocapnic condition.…”

Section: Mri Analysesmentioning

confidence: 99%

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Is High Blood Pressure Self-Protection for the Brain?

Warnert

Rodrigues

Burchell

et al. 2016

Circulation Research

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H igh blood pressure (BP) affects ≈25% of the world's population and is the largest single contributor to global mortality. 1 Hypertension represents a significant economic burden to public healthcare providers, where the global cost of nonoptimal BP is estimated to be US$370 billion (10% of healthcare expenditure). 2Remarkably, despite the availability of many pharmacological treatments, BP is poorly controlled with a recent report stating that only 53% of patients prescribed antihypertensive medication have BP controlled.3 This reflects the well-known heterogeneity of the syndrome, including epigenetic and inherited factors contributing to the unknown causes in 95% of patients. Despite the devastating consequences of hypertension (eg, stroke, kidney failure, coronary heart disease, and death 1,2 ), the mechanisms that lead to the onset of hypertension in humans are poorly understood. It is well established that elevated sympathetic nerve activity (SNA) contributes to the development of hypertension in most humans, [5][6][7] but what initiates this remains unclear. Experimental data from hypertensive rats and observations in postmortem human studies suggest that blood flow to the brain might be important in setting the operating level of SNA and, thus, systemic arterial pressure. Rationale: Data from animal models of hypertension indicate that high blood pressure may develop as a vital mechanism to maintain adequate blood flow to the brain. We propose that congenital vascular variants of the posterior cerebral circulation and cerebral hypoperfusion could partially explain the pathogenesis of essential hypertension, which remains enigmatic in 95% of patients.Objective: To evaluate the role of the cerebral circulation in the pathophysiology of hypertension. Methods and Results:We completed a series of retrospective and mechanistic case-control magnetic resonance imaging and physiological studies in normotensive and hypertensive humans (n=259). Interestingly, in humans with hypertension, we report a higher prevalence of congenital cerebrovascular variants; vertebral artery hypoplasia, and an incomplete posterior circle of Willis, which were coupled with increased cerebral vascular resistance, reduced cerebral blood flow, and a higher incidence of lacunar type infarcts. Causally, cerebral vascular resistance was elevated before the onset of hypertension and elevated sympathetic nerve activity (n=126). Interestingly, untreated hypertensive patients (n=20) had a cerebral blood flow similar to age-matched controls (n=28). However, participants receiving antihypertensive therapy (with blood pressure controlled below target levels) had reduced cerebral perfusion (n=19). Finally, elevated cerebral vascular resistance was a predictor of hypertension, suggesting that it may be a novel prognostic or diagnostic marker (n=126). Conclusions:

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Section: Discussionmentioning

confidence: 99%

Section: Mri Analysesmentioning

confidence: 99%

Is High Blood Pressure Self-Protection for the Brain?

Warnert

Rodrigues

Burchell

et al. 2016

Circulation Research

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“…To assess the effect of SNP on cerebrovascular conductance, a cerebrovascular conductance index was calculated as MCA V mean divided by mean IAP. 18 Changes in systemic and cerebral hemodynamics elicited by SNP were expressed as averages of 3-minute episodes of mean IAP, HR, SV, CO, SVR, MCA V mean , and cerebrovascular conductance index determined at 3 moments: before SNP treatment, midway through treatment, and when target BP was reached.…”

Section: Discussionmentioning

confidence: 99%

Impaired Cerebral Autoregulation in Patients With Malignant Hypertension

et al. 2004

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Background-In patients with a malignant hypertension, immediate parenteral treatment with blood pressure-lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. Methods and Results-In 8 patients with mean arterial pressure (MAP) Ͼ140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA V mean to MAP phase lead and static CA as the MCA V mean to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA V mean to MAP phase lead was lower (30Ϯ8°versus 58Ϯ5°, meanϮSEM; PϽ0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA V mean decrease was 22Ϯ4%, along with a 27Ϯ3% reduction in MAP (from 166Ϯ4 to 121Ϯ6 mm Hg; PϽ0.05) in a linear fashion (averaged slope, 0.82Ϯ0.15% cm · s Ϫ1 · % mm Hg

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“…Beat-to-beat MCA V m, Vs, and Vd were measured as well as MCA PP V (MCA PP V ϭ MCA Vs Ϫ MCA Vd). The cerebrovascular conductance index (CVCI) was calculated by dividing MCA V m by MAP and used as an estimate for changes in cerebrovascular conductance (23). MAP at the level of the MCA took into consideration the vertical distance from the fourth intercostal space in the midclavicular line (heart level) to the transcranial Doppler probe (i.e, hydrostatic pressure ϭ vertical distance ϫ 0.77 mmHg/cm).…”

Section: Methodsmentioning

confidence: 99%

Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans

Ogoh

Fadel

Zhang³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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107

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Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans. Am J Physiol Heart Circ Physiol 288: H1526 -H1531, 2005. First published December 9, 2004; doi:10.1152/ajpheart. 00979.2004.-Exercise challenges cerebral autoregulation (CA) by a large increase in pulse pressure (PP) that may make systolic pressure exceed what is normally considered the upper range of CA. This study examined the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) and systolic (V s), diastolic (Vd). and mean (Vm) middle cerebral artery (MCA) blood flow velocity during mild, moderate, and heavy cycling exercise. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated using transfer function analysis. PP increased by 37% and 57% during moderate and heavy exercise, respectively (P Ͻ 0.05), and the pulsatility of MCA V increased markedly. Thus exercise increased MCA V m and Vs (P Ͻ 0.05) but tended to decrease MCA V d (P ϭ 0.06). However, the normalized low-frequency transfer function gain between MAP and MCA V m and between SBP and MCA Vs remained unchanged from rest to exercise, whereas that between DBP and MCA V d increased from rest to heavy exercise (P Ͻ 0.05). These findings suggest that during exercise, CA is challenged by a rapid decrease rather than by a rapid increase in blood pressure. However, dynamic CA remains able to modulate blood flow around the exercise-induced increase in MCA V m, even during high-intensity exercise. cerebral circulation; diastolic velocity; systolic velocity CEREBRAL AUTOREGULATION (CA) maintains steady-state cerebral blood flow relatively stable over a range of perfusion pressures from 60 to 150 mmHg (21), but it takes ϳ3 s for CA to be established (1), explaining why the velocity (V) in basal cerebral arteries fluctuates in parallel with blood pressure throughout the cardiac cycle. Thus exercise presents a challenge to CA by the rapid and large increases in pulse pressure (PP). This is exemplified during rowing where the rapid fluctuations in blood pressure associated with each stroke result in similar fluctuations in middle cerebral artery (MCA) mean blood flow velocity (V m ) (17). Equally, during rhythmic resistance exercise fluctuations in arterial pressure with each muscle contraction are too rapid to be countered by CA (9). Despite such large changes in the MCA V waveforms with exercise, the averaged MCA V m remains unchanged (9), slightly decreased (7), or increased when exercise does not cause large fluctuations in blood pressure (3,16,17). However, the MCA V m may not fully reflect the dynamic control of CA (15,24,26,27), and this may be relevant especially when PP increases systolic pressure beyond the CA range.Dynamic CA is frequency dependent (10,15,24,26,27), and frequency-domain analyses of CA allows for evaluation of the influence of exercise-induced changes in arterial blood pressure on MCA V. Brys et al. (3) used frequency-domain analysis to ev...

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Cerebral Hemodynamics During the Valsalva Maneuver

Cited by 85 publications

References 17 publications

Is High Blood Pressure Self-Protection for the Brain?

Is High Blood Pressure Self-Protection for the Brain?

Impaired Cerebral Autoregulation in Patients With Malignant Hypertension

Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans

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