Cerebral hemodynamics during graded Valsalva maneuvers.

Blake G Perry,Samuel J E Lucas,Toby Mã¼Ndel,James D Cotter,Gaizka Mejuto

doi:10.3389/fphys.2014.00349

Abstract

The Valsalva maneuver (VM) produces large and abrupt changes in mean arterial pressure (MAP) that challenge cerebral blood flow and oxygenation. We examined the effect of VM intensity on middle cerebral artery blood velocity (MCAv) and cortical oxygenation responses during (phases I–III) and following (phase IV) a VM. Healthy participants (n = 20 mean ± SD: 27 ± 7 years) completed 30 and 90% of their maximal VM mouth pressure for 10 s (order randomized) whilst standing. Beat-to-beat MCAv, cerebral oxygenation (NIRS) and MAP across the different phases of the VM are reported as the difference from standing baseline. There were significant interaction (phase * intensity) effects for MCAv, total oxygenation index (TOI) and MAP (all P < 0.01). MCAv decreased during phases II and III (P < 0.01), with the greatest decrease during phase III (−5 ± 8 and −19 ± 15 cm·s−1 for 30 and 90% VM, respectively). This pattern was also evident in TOI (phase III: −1 ± 1 and −5 ± 4%, both P < 0.05). Phase IV increased MCAv (22 ± 15 and 34 ± 23 cm·s−1), MAP (15 ± 14 and 24 ± 17 mm Hg) and TOI (5 ± 6 and 7 ± 5%) relative to baseline (all P < 0.05). Cerebral autoregulation, indexed, as the %MCAv/%MAP ratio, showed a phase effect only (P < 0.001), with the least regulation during phase IV (2.4 ± 3.0 and 3.2 ± 2.9). These data illustrate that an intense VM profoundly affects cerebral hemodynamics, with a reactive hyperemia occurring during phase IV following modest ischemia during phases II and III.

Highlights

The Valsalva maneuver (VM) is commonly recruited during everyday activities such as lifting (Mac Dougall et al, 1992), defecation and coughing (Hamilton et al, 1944), and is characterized by changes in intrathoracic pressure that have a pronounced effect on venous return, cardiac output and blood pressures (Tiecks et al, 1995)
We examined the effect of VM intensity on middle cerebral artery blood velocity (MCAv) and cortical oxygenation responses during and following a VM
Phase I of the VM is characterized by an increase in mean arterial blood pressure (MAP) at the onset of strain as the elevated intrathoracic pressure is translated to the arterial circulation; during phase IIa a reduction in atrial filling pressure decreases stroke volume with a baroreflex-mediated recovery in blood pressure, via an increased heart rate; phase III features a rapid decline in MAP as the strain is released, and; phase IV has a rapid recovery and overshoot of MAP as the restored cardiac output is ejected into a constricted systemic vasculature (Goldberg et al, 1952; Tiecks et al, 1995; Pott et al, 2000)

Summary

Introduction

The Valsalva maneuver (VM) is commonly recruited during everyday activities such as lifting (Mac Dougall et al, 1992), defecation and coughing (Hamilton et al, 1944), and is characterized by changes in intrathoracic pressure that have a pronounced effect on venous return, cardiac output and blood pressures (Tiecks et al, 1995). The abrupt reduction in MAP during phase III challenges the regulation of cerebral perfusion and can result in syncope (Duvoisin, 1961) even after brief (10 s) VMs when standing (Perry et al, 2014). Whilst more intense VMs produce greater reductions in cerebral blood flow (CBF) velocity during Phase III (Perry et al, 2014), it is not known whether these fluctuations in flow coincide with changes in oxygenation

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