Abstract
Intrathoracic pressure influences cardiac output and may affect cerebral blood flow (CBF). We aimed to quantify the cerebral hemodynamic response to intrathoracic pressure reduction in patients with acute ischemic stroke using a noninvasive respiratory impedance (RI) device. We assessed low-level (6 cm H(2)O) and high-level (12 cm H(2)O) RI in 17 spontaneously breathing patients within 72 h of anterior circulation acute ischemic stroke. Average age was 65 years, and 35% were female. Frontal lobe tissue perfusion and middle cerebral artery velocity (MCAv) were continuously monitored with optical diffuse correlation spectroscopy (DCS) and transcranial Doppler ultrasound, respectively. High-level RI resulted in a 7% increase in MCAv (p = 0.004). MCAv varied across all studied levels (baseline vs low-level vs high-level, p = 0.006), with a significant test of trend (p = 0.002). Changes were not seen in DCS measured tissue perfusion by nonparametric pairwise comparison. Mixed effects regression analysis identified a small increase in both MCAv (low-level RI: β 2.1, p < 0.001; high-level RI: β 5.0, p < 0.001) and tissue-level flow (low-level RI: β 5.4, p < 0.001; high-level RI: β 5.9, p < 0.001). There was a small increase in mean arterial pressure during low-level and high-level RI, 4% (p = 0.013) and 4% (p = 0.017), respectively. End-tidal CO(2) remained stable throughout the protocol. RI was well tolerated. Manipulating intrathoracic pressure via noninvasive RI was safe and produced a small but measurable increase in cerebral perfusion in acute ischemic stroke patients. Future studies are warranted to assess whether RI is feasible and tolerable for prolonged use in hyperacute stroke management.