Post cardiac arrest (CA) syndrome is a severe condition associated with high mortality and significant long-term disabilities among survivors, mainly because of brain injury. Whether alterations in brain hemodynamics after the return of spontaneous circulation significantly contribute to this injury remains controversial. Pressure cerebral autoregulation (CaR) is an intrinsic cerebral arteriolar homeostatic mechanism that regulates cerebral blood flow (CBF) during fluctuations in cerebral perfusion pressure (CPP) by responding with vasoconstriction or vasodilation to increased or decreased CPP, respectively. CaR is altered in survivors of CA, and its alterations correlate to outcome [1]. Arterial partial pressure of carbon dioxide (PaCO2) also influences the cerebrovascular tone directly through modifications in perivascular pH, determining cerebral vasoconstriction or vasodilation in case of hypocapnia or hypercapnia, respectively. Such modification in the cerebrovascular tone could potentially affect CaR efficiency; however, this issue remains controversial.
The aim of this study was therefore to evaluate the effect of PaCO2 changes on CaR in patients with CA. We included consecutive adult patients with CA (> 18 year) who were admitted to our intensive care unit (January 2017 to January 2019) and were treated with targeted temperature management (TTM) at 33 °C for 24 h. Exclusion criteria were CA due to trauma, sepsis, intoxication, or acute intracranial disease; severe hypotension (i.e., mean arterial pressure < 55 mm Hg); cardiac arrhythmias; known supraaortic vascular disease; mechanical cardiac support; and contraindication to PaCO2 manipulation (i.e., signs of elevated intracranial pressure). All patients were mechanically ventilated; sedation and neuromuscular blocking agents (NMBAs) were provided as needed. CaR was assessed during hypothermia consecutively at two different PaCO2 levels using the mean flow index (Mxa). Mxa is a transcranial Doppler (TCD)-derived index of CaR that uses arterial blood pressure (ABP) as a surrogate for CPP and modifications in blood flow velocity (FV) of the middle cerebral artery (MCA) as a surrogate of CBF fluctuations. Mxa ranges from − 1 to + 1, with a lower value indicating better CaR; impaired CaR is generally identified by an Mxa > 0.3. TCD was performed on the left or right MCA. MCA FV and ABP were recorded simultaneously (DWL, Germany), and Mxa was calculated using MATLAB (MathWorks, USA), as previously explained [2]. After the first TCD recording, the respiratory rate was modified to decrease minute ventilation in order to modify PaCO2. An arterial blood gas analysis was performed every 15 min until a steady difference in PaCO2 of at least 7 mm Hg was achieved and Mxa was repeated; PaCO2 was measured using the “alpha-stat” (i.e., temperature-uncorrected values). Two Mxa values, one at low PaCO2 (lCO2 = 30–40 mm Hg) and another at high PaCO2 (hCO2 = 41–50 mm Hg) level, were therefore obtained for each patient. A Cerebral Performance Category score of 3–5 at 3 months defined unfavorable neurological outcome (UO). Statistical analysis was performed using IBM SPSS 24.0; continuous variables were expressed as median [25th–75th percentiles], and categorical variables were expressed as count (percentage). The Kruskal–Wallis test was used to compare repeated measurements over time. The study was approved by the institutional review board (410429000).
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