Abstract
In patients with acute ischemic stroke, penumbral perfusion is maintained by collateral flow and so far is maintained by normal mean arterial pressure (MAP) levels. Since MAP is dependent on cardiac function, optimization of cardiac output might be a valuable hemodynamic goal in order to optimize cerebral perfusion (CP). Cerebral perfusion was assessed by transcranial color-coded duplex and transcranial perfusion sonography in 10 patients with acute large hemispheric stroke. Time-to-peak (TTP) values of defined regions of interest (ROI) within the middle cerebral artery (MCA) territory were assessed bilaterally in addition to mean flow velocities of the MCA. Via semi-invasive advanced hemodynamic monitoring systemic hemodynamic parameters were assessed, including MAP and cardiac index (CI). Patients received sonographic follow-up after optimizing CI. TTP values of the deeply located ROIs of the non-affected as well as the affected hemisphere correlated highly significantly with CI (in affected side r = -0.827, p = 0.002; and in non-affected side r = -0.908, p < 0.0001). This demonstrates dependence of CP on CI, while correlation with MAP was not detected. Neither CI nor MAP revealed significant correlation with MCA velocity.
Highlights
Restoring penumbral perfusion is the key target of therapeutic efforts in acute ischemic stroke
mean arterial pressure (MAP) is expected to be related to cerebral perfusion (CP), as constant cerebral blood flow (CBF) is maintained over a wide range of MAP due to vessel autoregulation [3]
MAP is expected to correlate with cardiac output (CO), since MAP is the product of CO and systemic vascular resistance [SVR; [4]]
Summary
Restoring penumbral perfusion is the key target of therapeutic efforts in acute ischemic stroke. In cases of insufficient or unsuccessful vessel recanalization, maintaining normal to higher mean arterial pressure (MAP) is the goal to preserve penumbral perfusion. MAP is expected to be related to cerebral perfusion (CP), as constant cerebral blood flow (CBF) is maintained over a wide range of MAP due to vessel autoregulation [3]. MAP is expected to correlate with cardiac output (CO), since MAP is the product of CO and systemic vascular resistance [SVR; [4]]. Former studies have demonstrated that MAP levels’ correlation to CO are volume state dependent, CP Depends on CO and CO might be a better parameter to focus on [4,5,6] since CBF depends on CO rather than on MAP in areas with impaired autoregulation [7]. Further influencing factors may change CO levels, for example, atrial fibrillation or medication [8]
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